VEGETABLE OIL PRODUCTION

INTRODUCTION

Vegetable oil is a triglyceride extracted from a plant. According to Wikipedia, the term "Vegetable oil" can be narrowly defined as referring only to plant oils that are liquid at room temperature or broadly defined without regard to a substance's state of matter at a given temperature. Hence vegetable oils that are solid at room temperature are sometimes called vegetable fat. In contrast to triglycerides, vegetable waxes lack glycerin in their structure. Many plant parts may produce oil, but in commercial practice oil is extracted primarily from seeds.

oils extracted from plants have been used since ancient times and in many cultures(Wikipedia). Many vegetable oils are consumed directly, or indirectly as ingredients in the food. Many vegetable oils are used as ingredient or component in many manufactured products; soaps, candles, perfumes, cosmetic products, etc.

However, one problem with using vegetable oils for industrial purposes is that they are susceptible to becoming rancid. Thus, oils that are more stable, like mineral oil or Ben oil are preferred over vegetable oil for industrial uses.

PRODUCTION

Production process of vegetable oil involves the removal of oil from plant components, mainly/typically seeds. There are two methods of vegetable oil extraction namely; chemical extraction using a solvent and mechanical extraction using oil mill. The oil extracted can then be purified (and refined, if need be) or chemically altered. Example of oils produced by chemical extraction include industrial oils such as soyabean oil and corn oil. And vegetable oils produced by mechanical means include the more traditional oils such as olive oil, coconut oil, etc.

PRODUCTION OF INSECTICIDE IN THE COMFORT OF YOUR HOME

INSECTICIDE -- DEFINITION AND USES

 Insecticide is a substance used to kill insects. They include 

ovicides and larvicides used against insect eggs and larvae, respectively. Insecticides are used in agriculture, medicine, industry and by consumers. Insecticides are claimed to be a major factor behind the increase in agricultural 20th century's productivity. Nearly all insecticides have the potential to significantly alter ecosystems; many are toxic to humans; some concentrate along the food chain.

Insecticides can be classified in two major groups namely: systemic insecticides(which have residual or long term activity) and contact insecticides(which have no residual activity).

Furthermore, one can distinguish three types of insecticide as follows:

1.Natural insecticides,such as nicotine, pyrethrum and neem extracts, made by plants as defenses against insects. 

2. Inorganic insecticides, which are metals. 

3. Organic insecticides, which are organic chemical compounds, mostly working by contact.

You can produce your own insecticide at home for use or for sale using the following steps.

N/B: Quantities of the chemical to be used depends on the amount of insecticide you intend to produce, but the major materials are the same.

A.  CHEMICALS

1. D. FORCE (D.D.V.P.)
2. INDUSTRIAL CAMPHOR
3. KEROSENE
4. FORMALIN

COMPOSITION FOR ONE LITRE OF INSECTICIDE

1. 75cl of Kerosene
2. 200g of Industrial Camphor
3. 10mls of Formalin
4. 25cl of D.D. Force

PREPARATION

1. Put the 75cl of Kerosene in a bottle
2. Add 25cl of D.D. Force
3. Add 200g of Industrial Camphor
4. Finally, add 10mls of Formalin
5. Mix together vigorously
6. Pour into your packaging materials
7. Cover it up with caps and label it.

B.  CHEMICALS

1. D.D Force/Mulvap 

2. Sniper

3. Industrial camphor

4. Formalin

5. Kerosene

6. IPA

7. Color

COMPOSITION FOR 5 LITRES OF INSECTICIDE(It depends on how strong you want the insecticide to be)

1. D.D Force/Mulvap ———- (125cl)
2. Sniper ——————  1000g 
3. Industrial Camphor – ——- 2kg
4. Formalin——————— 1/2 (But use 1/16, to avoid Formalin peppering one’s eyes. 
5. Kerosene——————– 5 Liters
6. IPA ————————- 1/2 Liter
7. Color ———————— As Desired (you can do without it)
8. Perfume ——————– As Desired (same; it is by choice)

Step 1: Pour the Kerosene into a big bowl, enough to allow stirring.

Step 2: Pour all the Industrial Camphor into the Kerosene for at least 30 minute or more before production. This is to enable it devolve properly in the Kerosene.

Step 3: Carefully pour the Mulvap into the kerosene

Step 4: Carefully pour the Sniper into the kerosene too

Step 5: Add all the IPA

Step 6: Add Perfume to satisfaction

Step 7: Add Color to satisfaction

NOTE: The color you be dissolved in water first before adding it to the mixture.

NACA/NCDC'S RESPONSE TO PROF. EZEIBE'S CLAIMS ON THE PRODUCTION OF DRUG THAT CURE HIV/AID IN NIGERIA

THE CLAIM ON DISCOVERY OF HIV/AIDS DRUG IN NIGERIA

A professor of Veterinary Medicine and Clinical Virology with Michael Okpara University of Agriculture, Umudike, in Abia, has detailed how he confirmed a drug that can cure HIV/AIDS which he discovered.

The varsity don, Prof. Maduike Ezeibe, gave the explanation while addressing newsmen, following the unveiling of a drug confirmed to wipe out traces of the virus in human by the Vice Chancellor of the University, Prof. Francis Otunta.

Prof. Ezeibe disclosed that the drug was produced with Aluminum Silicate and Magnesium Silicate (Synthetic Aluminum-Magnesium Silicate).

He said that the two minerals “are already in use as medicines for the treatment of various animal and human diseases.”

“10 persons living with the disease ‘who volunteered’ were made to apply through their doctor to the VC.

“They were treated daily with the Medicinal Synthetic Aluminum-Magnesium Silicate (50 mg/kg),

The volunteers were subjected to monthly tests for viral loads and CD4-lymphocyte counts.

“With the antiviral effects of the medicine, its ability to reach all cells (as nanoparticles) and the lymphocytes, there is no more hiding place (sanctuary) for HIV,” he said.

Ezeibe also said that he presented the research findings to the World Virology Conference in Atlanta in 2015, and Antonio (Texas) in 2016.

Besides, he said that the results of the laboratory tests had been published in many international scientific journals, including the British Journal of Medicine and Medical Research, among several others.

"He said that he was also about to sign a memorandum of understanding with a U.S.-based Scientific Research Publishing, publishers of World Journal of AIDS, for the publication of his book “How I came about the cure for HIV/AIDS”.

He explained that the medicine had been used to potentiate Ampicillin, Chloroquine, Piperazine and Sulphadimidine, among others, and could be a major foreign exchange earner for Nigeria if approved by relevant authorities.

Ezeibe, who said that the medicine was patented in August 2014 in Nigeria, called on the Federal Government to help him to secure international patency for the drug.

According to him, “local and international pharmaceutical companies would find the product as a veritable raw material.”

“If commercialized, the Medicinal Synthetic Aluminum-Magnesium Silicate would become an alternative for petroleum to the Nigerian economy.”

REACTIONS TO THE CLAIM BY NACA AND NDCD

Our attention has been drawn to a recent media statement by Maduike Ezeibe, a Professor of Veterinary Medicine and Clinical Virology at the Michael Okpara University of Agriculture, claiming to have discovered a new drug for the cure of HIV/AIDS. An editorial in the newspaper “Leadership” (http://leadership.ng/opinions/569782/nigerian-scientist-conquers-hivaids), quoted the professor as saying that the drug, produced with “Aluminium Magnesium Silicate” was tested on ten persons living with HIV. The newspaper reported a clinical outcome of an ability to “reach all cells” and making HIV “a conquered organism”.

The claim for a HIV/AIDS cure is not new. It is also not new to find a scientist using ambiguous scientific methods and practices to buttress this claim, and to find obscure journals increasingly prepared to publish these claims. Following the discrediting of the claims of Dr Abalaka in the late nineties, we had also hoped that the Nigerian press would thoroughly investigate these “AIDS cure”, claims before going to press, given the huge impact that these could have on patients lives.

To examine the facts, this study was published in two little known, fee-charging ‘predatory’ journals and involved less than ten patients. In the “clinical trial” as reported, there was no evidence of the use of controls, which is the basis of all efficacy trials.  Without controls, you can neither have randomisation nor blinding, two other critical factors in studying the effects of new medicines.  Critically the primary outcome measured in this study was based on plasma viral load levels that are known to fluctuate in patients, even in the absence of any intervention. It is also worth noting that virological suppression (viral load less than 50 copies/ml) was not achieved in 6 of 8 patients. There appeared to be no medical doctor involved in the execution of this study and there was no evidence on where or how the patients were treated or monitored during this study, their clinical and treatment status at the beginning or at the end of it.

It is important to note that clinical trials are conducted in a series phases – each phase is designed to answer a separate research question. These include; 1.) Phase I: Researchers test a new drug or treatment in a small group of people for the first time to evaluate its safety 2.) Phase II: The drug or treatment is given to a larger group of people to see if it is effective 3.) Phase III: The drug or treatment is given to large groups of people to confirm its effectiveness, comparing it to commonly used treatments, and Phase IV: Studies are done to gather information on the drug’s effect in various populations and any side effects associated with long-term use. The authors of this study did not state what phase their study was and the results of previous phases, if these were done.

One critical issue is that there was no evidence from the publication that the authors obtained ethical clearance from an appropriate body in Nigeria to conduct this study, and only ambiguous evidence that informed consent was sought from the evidently vulnerable patients.

There is really no basis for a claim to cure of AIDS in this study.

We are concerned that the publicity given to these claims will stop patients with HIV from taking life-saving antiretrovirals and give them false hope of a cure. It will be a great disservice to this vulnerable group of patients for the media to disseminate these claims in the absence of sound scientific evidence. There are long established, tried and tested routes for the discovery, development and validation of modern medicines before they can be registered and used for treatment in humans and animals. We call on all academics to follow legal and scientifically acceptable methods in conducting their research and to avoid making premature claims that are capable of derailing the huge progress made in the last two decades on the war against HIV/AIDS. Millions of lives have been saved as a result of modern antiretroviral treatment and people living with HIV can now look forward to a normal healthy future. We continue to support the hard and diligent work being done by scientists in our Universities and research institutions around the country. We are always ready to partner with our scientists on all aspects of HIV research provided this is in line with international best practice.

We call on editors of media houses in Nigeria to seek comments from the leadership of the relevant government parastatals and professional bodies when it receives new research findings related to our areas of responsibility. We assure you that we will respond rapidly and constructively to any queries.  We also urge the editors of media houses in Nigeria to support their reporters to gain a deeper understanding of the complexities involved in the clinical trial process. In the run up to the next deadline, it is easy to fall into the trap of doing more harm than good, and the consequences of this can be deadly in the health sector. We will support the evolution of robust science journalism in Nigeria.

We call on all patients living with HIV that are currently taking their medications to continue to do so and to see their doctors if they have any concern. The NACA helpline (6222) is available on working days from 8am-8pm for members of the public seeking more information on HIV disease.

Signed

Dr Sani Aliyu

Director-General, National Agency for the Control of AIDS (NACA)

Dr Chikwe Ihekweazu

CEO Nigeria Centre for Disease Control (nCDC)

PRODUCTION OF LIQUID SOAP IN SHORT NOTE

MATERIALS AND STEPS FOR LIQUID SOAP PRODUCTION

Step 1 - Prepare all ingredients and tools for production. 

Step 2 -Dissolve caustic soda and soda ash in water and stir. 

Step 3 -Dissolve CMC in a separate bowl and stir. 

Step 4 - Mix the Texapon and the Sulphuric acid and stir.

Step 5 - Add the dissolved caustic and soda ash to the dissolved CMC and stir. 

Step 6 - Add dissolved texapon and surphonic acid to the CMC mixture and stir. 

Step 7 - Pour Glycerin into the mixture and stir. 

Step 8 - Add the formalin to the mixture and stir. 

Step 9 - Mix your colorant and stir until the colour is evenly distributed. 

Step 10 - Allow the mixture to settle for 45 minutes to 1 hour. 

Step 11 - Add perfume to mixture and stir 

Step 12 - Add the booster to mixture and stir.

Step 13- Add water and stir until you get the desired consistency. 

Step 14 -Cover the mixture and allow to sit for 24hours before packaging for sale. 

Note: To produce 25 liters of liquid soap: • Use 10 liters of water to dissolve the CMC • Use 10 liters of water to dissolve the caustic soda and soda ash • Add approximately 5 liters of water while mixing to get the desired consistency. • You may add extra water to make the liquid soap more and lighter if you are selling to customers like road side restaurant owner

PURE WATER PRODUCTION IN NIGERIA

PURE WATER BUSINESSES

Water is one of the most essential thing for human survival. In as much as it looks abundant, safe and portable drinking water seems scarce. For that reason, processing and packaging of water for sell is a huge business, as its demand almost equal to the population of a given place. However, bring a consumable goods, extreme care should be taken in its ptoduction. Sachet Water (Pure Water as it is popularly called in Nigeria) is lucrative in Nigeria, as it is very portable and affordable.

REQUIREMENTS FOR PURE/SATCHET WATER PRODUCTION

1. Get a place of business – You need to acquire or rent a place for your pure water business, depending on your budget or available capital. If you have the capital, acquiring your own property and developing it is the most desirable option as that will save you cost in the long run.

2. Branding -- Branding is very important in business, so in addition to your business name, design a very professional logo for your product because how people see it determines its marketability. Make your brand the best among equals. 

3. Register your business name – Get the name of your company and product registered with the right people in charge of business registration. 

4. Sink a Borehole – The most common source of water for commercial drinking water production like sachet water and bottled water is borehole, let there be borehole within your premises for constant water supply to your pure water production factory.

5. Install Overhead Tanks – This will serves as reservoir to supply water to the distillation system, it has to be overhead to ensure proper pressure to be able to pump down the distillation chamber.

6. Install Distillation System – This could just be a micro filters and cup filters depending on your start up capacity, but if you can afford it, then you go for more comprehensive distillation system. Otherwise, use Purification process known as Ultra Violet sterilization bulbs process. After distillation, you need to take your product (the resultant water) to the laboratory for results.

7. Get NAFDAC Approved –  As a legal business, one should register and get approval from NAFDAC(agency in charge of making sure that consumable goods in Nigeria are safe for consumption) for his or her pure water business.

8. Buy appropriate Machine:  In the production of satchet water(pure water), the two important equipment needed for production are water treatment plant and satchet water filling machine. Also automatic sealing machine is required. You should buy automatic sealing machine that seals most number of satchet water per minute.

9. Employ Staffs – Minimum of 4 - 6 persons to work in your factory for a start then increase with time as the demand may be.

10. Distribution Mechanism – Buy truck for your distribution of rent but renting can be expensive and disappointing most of the times. My recommendation is that you buy your own truck if you can afford it at the beginning.

12. Get Power Generation – Due to the erratic power supply one presently experiences in the country, it is highly advisable to have. If a standby power generating set;  25KVA generator will serve you for the business.

MARKET INSIGHT
*  The market for sachet and bottle water is national .With a population of over one hundred and forty million (140,000,000) people and an estimated national population growth rate of 5.7% per annum , average economic growth rate of 3.5% per annum in the past five (5) years ,Nigeria is a large ,expanding and sustainable market for sachet and bottle water. Though the market for sachet and bottle water in Nigeria, the business tends to sale more in the northern part of Nigeria where hot weather is prompting people into drinking more water than usual and lack of clean pump water contributed in giving the business a good push up.

*  Sachet and bottle water is consumed on daily basis by all and sundry irrespective of age, social class or religion. The raw material required for the production of sachet water is water while the other factors of production like land, capital, labour also comes to play.

*  The return on this project is quite attractive and impressive that it would be difficult for any financial institution especially banks with discerning credit officers to turn down any loan request for funding this project. Promoters of this venture will also feel comfortable to release their hard earned money to finance this project.

*  The successful implementation of this project begins with the preparation of detailed and bankable feasibility study report to ascertain the actual cost/benefit status of the project. As a part of the legal requirements, the promoter has to register its product with NAFDAC.

AROUND THE GLOBE: The Originality Of The World : BASIC THINGS TO KNOW BEFORE LEARNING HOW TO SEW A CLOTH

AROUND THE GLOBE: The Originality Of The World : BASIC THINGS TO KNOW BEFORE LEARNING HOW TO SEW A CLOTH

AROUND THE GLOBE: The Originality Of The World : BROOM BUSINESS IN NIGERIA

AROUND THE GLOBE: The Originality Of The World : BROOM BUSINESS IN NIGERIA

BROOM BUSINESS IN NIGERIA

Broom making and selling is a lucrative business in Nigeria; virtually every home, office place, etc use broom for keeping the surroundings clean. Those in the industry have testify how good the business is.

According to report, a marketer said that what motivates him to remain in the broom selling business despite the introduction of electronic sweepers and the fibre brushes, Udo was that it is rewarding. In his words:  “The business goes beyond what you see. In fact, a potential seller does not just go into it. He needs to go through years of apprenticeship because the trade is in phases. You first must know how to preserve, then sourcing and then the distribution. If you preserve them badly, in moist places, they will be brittle and become unprofitable. So, one has to know the right temperature for it."

“The hover machines and fibre brushes cannot be compared to palm frond brooms. Unlike hover machines, which are powered by electricity, the broom does not need that and they are cheaper if you compare them’s in term of maintenance and repairs. Besides, the market is huge; I at times leave Lagos to Abeokuta and other states in the West to sell brooms. We make different brooms, the long ones for sweeping open spaces, the medium for the rooms, the short ones for ladies that prepare Ewedu soup and the extreme short for washing potties; and their prices are not the same. I make between N150 to N200 as profit from a bunch of broom sold. In a month I make between N80,000 to N100,000,” he disclosed."  Wah!
They source for finished product from various villages where they are produced in large quantities. Getting the quantity needed, the tie them into smaller bunches with raffia thread or plastic tapings and sell to buyers. The prices vary from one place to the other, and no matter the location one is sure to make good profit. According to a seller, "For each little bunch that goes for N200, I make N80 and multiply that into a 1000 in a month. However, this price differs from place to place; for instance the same broom could go for N300 or more at Ikoyi or Lekki. Only we make them look attractive and different from your every day broom by dying the head or handle with different colours and also add a pole to some, so that one can use them to clean the ceiling or high places in a house while standing,” 

The add colour to the brooms to add more value, thus attracting more money per broom. A marketer said “We add colours and sell them higher because people like flashy things. Also, we make the colours to be in line with the APC party, whenever we are in APC dominated state, so that party faithful can get their brooms from us,” 

The level one wants to begin would determine the capital outlay. The start-up capital could be as low as N10,000. If you want to be on the street hawking or at particular junctions, it means with N10,000 to N20,000 one can venture into it. But if one wants to go to the villages or the remote areas to get them, then one would need a huge capital to buy the brooms from the people doing it and if possible commission the locals, who are mostly youths and women.

“I started by hawking, carrying brooms in a wheelbarrow from street to street, and gradually moved to travelling to Benin, Akure and other places with a lot of palm trees to get brooms. I sell more in the cities, despite fibre brushes. Some people believe no other item can sweep their homes cleaner than the palm frond brooms. On the average, I make N60,000 to N80,000 selling as a retailer and whole seller. The profit margin is high. I get the bunch for a very low price, sometimes N100, depending on the location and sometimes less and after retying each bunch, sometimes I make N2,000. And I do get such bunches in hundreds."

“The business is flexible and anyone that knows packaging would make quick money within a short time. I do not regret being in the business because it has paid my bills,”

Some of the challenges in the business:
bad roads and weather as the major constraints; bad roads make it difficult for one to sometimes go into the remote areas, while rainy season hampers the brooms making because it would be difficult to climb the palm trees for the fronds and also for the sun to properly dry the sticks.

Advice:
One should get a mini-warehouse to store the products so that during the rains sellers and buyers would still have wares to sell and buy.

BASIC THINGS TO KNOW BEFORE LEARNING HOW TO SEW A CLOTH

There are many reasons why people learn how  to make clothes in Nigeria. It ranges from financial needs to personal needs.

Learn the different tools you'll need. 

Making clothes requires a bunch of different tools for sewing, for making patterns, and for measuring the patterns to make sure that they will fit you. You will need to learn each type of tool and how to use it. In the beginning you won't be comfortable with all the tools, but the more you practice, the easier it will become.

• Iron and ironing board. It's fine to use whatever quality iron you already have, but you'll probably want to eventually invest in a higher quality one. You'll be using the iron to press the item being sewn as you are sewing as this makes sure the seams stay open properly.
• Seam ripper. You'll use this when you've made a mistake to rip out the wrong stitches.
• Chalk for marking the fabric so you know where to sew and where to cut.
• You'll need a really nice, sharp pair of scissors that you designate for cutting cloth only, otherwise the scissors will dull more quickly and can damage or fray your fabric.
• Tracing paper for drafting your patterns and modifying the patterns as you're sewing.
• Rulers for drafting and measuring while you're constructing your piece (both in the design stages and the sewing stages).
• Tape measuring, especially a flexible tape measure. You'll use this to take measurements and make fit adjustments if you need them.
• Pins for holding the fabric in position before you start sewing. Pins should be used only sparingly as they can distort the fabric that you're working with.

Acquire a sewing machine. 

There are basically two types of sewing machines, ones that fall into the household/domestic category and ones that fall into the industrial use category. There are pros and cons to both of these categories so it will take a little deciding to figure out which will work best for your needs.

• Household sewing machines tend to be more portable and more versatile. They tend to do a variety of stitch types. However, they don't work out as well in terms of speed and power, and they aren't very good with heavy fabrics.
• Industrial sewing machines are much more powerful and much faster, but they tend to only be able to do one type of stitch (such as a straight lockstitch). They do that one stitch very well, but aren't terribly versatile. They also tend to take up a lot more room
• 
  

Learn the parts of your sewing machine. 

Hopefully your sewing machine will come with an instruction manual, because that will tell you which direction the bobbin is going to spin and where the bobbin case is. However, you're going to need to know at least the basic components of your sewing machine before you can get making fun things.

• The spool holder holds the spool of thread and controls the direction of the thread while it goes through the sewing machine. Depending on the type of machine you have, your spool holder might be horizontal or it might be vertical.
• Bobbin is basically a spindle that is wound with thread. You have to wind the bobbin with thread and fit it into the bobbin case (which is found under the needle plate).
• Your sewing machine also has different stitch adjustments to help determine stitch length for each stitch, the amount of tension needed to make sure the stitches come through properly, and the different types of stitches (if you have the type of sewing machine that does different stitch types).
• The take up lever controls the thread tension. If the thread tension isn't at its proper level the threads will knot up, jamming the sewing machine.
• You can check with a nearby sewing shop to see if they have any classes or know anyone willing to help you get set up with your sewing machine, or you can ask a knowledgeable family member or friend.

HIV AND AIDS: HISTORY, RESEARCH AND DISCOVERIES

INTRODUCTION

HIV/AIDS awareness initiative is a collective responsibility that is not limited to the health sector, but to all and sundry. It could be termed a global crisis " with victims all around the entire globe(Adesoji and Olakekan). Inadequate information regarding the spread of this global disease could pose a devastating effect on economic growth and social sustainability of the whole world. Hence, creativity, synergy and collaboration from all sectors of society are required to finding solution to mitigate and curb the widespread. According to UNAIDS (2008) HIV/AIDS is among the greatest challenge facing economic growth, social and civil society development today; it is a global crisis that gradually destroys all aspect of society. No region of the world has been left out; the epidemic remains extremely dynamic, growing and changing characters as the virus exploit new opportunities for transmission. An epidemic as serious as HIV/AIDS needs innovative and global sensitization. Therefore, everybody should join hands towards committed, urgent and sustainable action(s) against this global enemy called HIV/AIDS.

Human immunodeficiency virus (HIV) attacks the body's immune system. A healthy immune system provides a natural defence against disease and infection. If the immune system is damaged by HIV, it increases the risk of developing a serious infection or disease, such as cancer.

According to HealthCentral Encyclopedia), HIV infects particular cells, called CD4 cells, that are found in the blood. CD4 cells are responsible for fighting infection. After they become infected, the CD4 cells are destroyed by HIV. Although the body will attempt to produce more CD4 cells, their numbers will eventually decline and the immune system will stop working.

HIV is spread through the exchange of bodily fluids. This most commonly happens during unprotected sexual contact, such as vaginal, oral and anal sex. People who inject illegal drugs and share needles are also at risk of catching HIV. The condition can also be spread from a mother to her unborn child.

There is no cure for HIV and no vaccine to stop you becoming infected. However, since the 1990s, treatments have been developed that enable most people with HIV to stay well and live relatively normal lives.

HIV is a special type of virus known as a retrovirus. The retrovirus reproduces inside the cell and releases copies of itself into the blood. It can be challenging to treat as the virus can rapidly mutate (alter) into new strains of virus.

Acquired immune deficiency syndrome (AIDS) is a term that is used to describe the late stage of HIV. This is when the immune system has stopped working and the person develops a life-threatening condition, such as pneumonia (infection of the lungs).

The term AIDS was first used by doctors when the exact nature of HIV was not fully understood. However, the term is no longer widely used because it is too general to describe the many different conditions that can affect somebody with HIV. Specialists now prefer to use the terms advanced or late-stage HIV infection.

HISTORY/ORIGIN:

False-color scanning electron micrograph of HIV-1, in green, budding from cultured lymphocyte

AIDS is caused by a human immunodeficiency virus (HIV), which was originated in non-human primates in Central and West Africa. While various sub-groups of the virus acquired human infectivity at different times, the global pandemic had its origins in the emergence of one specific strain – HIV-1 subgroup M – in Léopoldville in the Belgian Congo (now Kinshasa in the Democratic Republic of the Congo) in the 1920s.

Two types of HIV exist: HIV-1 and HIV-2. HIV-1 is more virulent, is more easily transmitted and is the cause of the vast majority of HIV infections globally. The pandemic strain of HIV-1 is closely related to a virus found in chimpanzees of the subspecies Pan troglodytes troglodytes, which live in the forests of the Central African nations of Cameroon, Equatorial Guinea, Gabon, Republic of Congo (or Congo-Brazzaville), and Central African Republic. HIV-2 is less transmittable and is largely confined to West Africa, along with its closest relative, a virus of the sooty mangabey (Cercocebus atys atys), an Old World monkey inhabiting southern Senegal, Guinea-Bissau, Guinea, Sierra Leone, Liberia, and western Ivory Coast.

Transmission from non-humans to humans

The majority of HIV researchers agree that HIV evolved at some point from the closely related simian immunodeficiency virus (SIV), and that SIV or HIV (post mutation) was transferred from non-human primates to humans in the recent past (as a type of zoonosis).[citation needed] Research in this area is conducted using molecular phylogenetics, comparing viral genomic sequences to determine relatedness.

HIV-1 from chimpanzees and gorillas to humans :

Scientists generally accept that the known strains (or groups) of HIV-1 are most closely related to the simian immunodeficiency viruses (SIVs) endemic in wild ape populations of West Central African forests. In particular, each of the known HIV-1 strains is either closely related to the SIV that infects the chimpanzee subspecies Pan troglodytes troglodytes (SIVcpz) or closely related to the SIV that infects western lowland gorillas (Gorilla gorilla gorilla), called SIVgor. The pandemic HIV-1 strain (group M or Main) and a rare strain found only in a few Cameroonian people (group N) are clearly derived from SIVcpz strains endemic in Pan troglodytes troglodytes chimpanzee populations living in Cameroon.[4] Another very rare HIV-1 strain (group P) is clearly derived from SIVgor strains of Cameroon.[7] Finally, the primate ancestor of HIV-1 group O, a strain infecting 100,000 people mostly from Cameroon but also from neighboring countries, has been recently confirmed to be SIVgor.[6] The pandemic HIV-1 group M is most closely related to the SIVcpz collected from the southeastern rain forests of Cameroon (modern East Province) near the Sangha River.[4] Thus, this region is presumably where the virus was first transmitted from chimpanzees to humans. However, reviews of the epidemiological evidence of early HIV-1 infection in stored blood samples, and of old cases of AIDS in Central Africa, have led many scientists to believe that HIV-1 group M early human center was probably not in Cameroon, but rather farther south in the Democratic Republic of the Congo, more probably in its capital city, Kinshasa (formerly Léopoldville).[4][10][11][12]

Using HIV-1 sequences preserved in human biological samples along with estimates of viral mutation rates, scientists calculate that the jump from chimpanzee to human probably happened during the late 19th or early 20th century, a time of rapid urbanisation and colonisation in equatorial Africa. Exactly when the zoonosis occurred is not known. Some molecular dating studies suggest that HIV-1 group M had its most recent common ancestor (MRCA) (that is, started to spread in the human population) in the early 20th century, probably between 1915 and 1941.[13][14][15] A study published in 2008, analyzing viral sequences recovered from a recently discovered biopsy made in Kinshasa, in 1960, along with previously known sequences, suggested a common ancestor between 1873 and 1933 (with central estimates varying between 1902 and 1921).[16] Genetic recombination had earlier been thought to "seriously confound" such phylogenetic analysis, but later "work has suggested that recombination is not likely to systematically bias [results]", although recombination is "expected to increase variance".[16] The results of a 2008 phylogenetics study support the later work and indicate that HIV evolves "fairly reliably".[16][17] Further research was hindered due to the primates being critically endangered. Sample analyses resulted in little data due to the rarity of experimental material. The researchers, however, were able to hypothesize a phylogeny from the gathered data. They were also able to use the molecular clock of a specific strain of HIV to determine the initial date of transmission, which is estimated to be around 1915-1931.[18]

HIV-2 from sooty mangabeys to humans

See also: HIV subtypes

Similar research has been undertaken with SIV strains collected from several wild sooty mangabey (Cercocebus atys atys) (SIVsmm) populations of the West African nations of Sierra Leone, Liberia, and Ivory Coast. The resulting phylogenetic analyses show that the viruses most closely related to the two strains of HIV-2 that spread considerably in humans (HIV-2 groups A and B) are the SIVsmm found in the sooty mangabeys of the Tai forest, in western Ivory Coast.[3]

There are six additional known HIV-2 groups, each having been found in just one person. They all seem to derive from independent transmissions from sooty mangabeys to humans. Groups C and D have been found in two people from Liberia, groups E and F have been discovered in two people from Sierra Leone, and groups G and H have been detected in two people from the Ivory Coast. These HIV-2 strains are probably dead-end infections, and each of them is most closely related to SIVsmm strains from sooty mangabeys living in the same country where the human infection was found.[3][12][19]

Molecular dating studies suggest that both the epidemic groups (A and B) started to spread among humans between 1905 and 1961 (with the central estimates varying between 1932 and 1945).[20] [21]

Bushmeat practice

According to the natural transfer theory (also called "hunter theory" or "bushmeat theory"), the "simplest and most plausible explanation for the cross-species transmission"[8] of SIV or HIV (post mutation), the virus was transmitted from an ape or monkey to a human when a hunter or bushmeat vendor/handler was bitten or cut while hunting or butchering the animal. The resulting exposure to blood or other bodily fluids of the animal can result in SIV infection.[22] Prior to WWII, some Sub-Saharan Africans were forced out of the rural areas because of the European demand for resources. Since rural Africans were not keen to pursue agricultural practices in the jungle, they turned to non-domesticated meat as their primary source of protein. This over-exposure to bushmeat and malpractice of butchery increased blood-to-blood contact, which then increased the probability of transmission.[23] A recent serological survey showed that human infections by SIV are not rare in Central Africa: the percentage of people showing seroreactivity to antigens—evidence of current or past SIV infection—was 2.3% among the general population of Cameroon, 7.8% in villages where bushmeat is hunted or used, and 17.1% in the most exposed people of these villages.[24] How the SIV virus would have transformed into HIV after infection of the hunter or bushmeat handler from the ape/monkey is still a matter of debate, although natural selection would favor any viruses capable of adjusting so that they could infect and reproduce in the T cells of a human host.

A study published in 2009 also discussed that bushmeat in other parts of the world, such as Argentina, may be a possible location for where the disease originated.[25] HIV-1C, a subtype of HIV, was theorized to have its origins circulating among South America.[25] The consumption of bushmeat is also the most probable cause for the emergence of HIV-1C in South America. However, the types of apes, shown to carry the SIV virus, are different in South America. The primary point of entry, according to researchers, is somewhere in the jungles of Argentina or Brazil.[25] An SIV strain, closely related to HIV, was interspersed within a certain clade of primates. This suggests that the zoonotic transmission of the virus may have happened in this area.[25] Continual emigration between countries escalated the transmission of the virus. Other scientists believe that the HIV-1C strain circulated in South America at around the same time that the HIV-1C strain was introduced in Africa.[25] Little research has been done on this theory because it is fairly young.

Emergence

Unresolved questions about HIV origins and emergence

The discovery of the main HIV / SIV phylogenetic relationships permits explaining broadly HIV biogeography: the early centers of the HIV-1 groups were in Central Africa, where the primate reservoirs of the related SIVcpz and SIVgor viruses (chimpanzees and gorillas) exist; similarly, the HIV-2 groups had their centers in West Africa, where sooty mangabeys, which harbor the related SIVsmm virus, exist. However these relationships do not explain more detailed patterns of biogeography, such as why epidemic HIV-2 groups (A and B) only evolved in the Ivory Coast, which is one of only six countries harboring the sooty mangabey.[citation needed] It is also unclear why the SIVcpz endemic in the chimpanzee subspecies Pan troglodytes schweinfurthii (inhabiting the Democratic Republic of Congo, Central African Republic, Rwanda, Burundi, Uganda, and Tanzania) did not spawn an epidemic HIV-1 strain to humans, while the Democratic Republic of Congo was the main center of HIV-1 group M, a virus descended from SIVcpz strains of a subspecies (Pan troglodytes troglodytes) that does not exist in this country. It is clear that the several HIV-1 and HIV-2 strains descend from SIVcpz, SIVgor, and SIVsmm viruses,[3][6][7][8][10][19] and that bushmeat practice provides the most plausible venue for cross-species transfer to humans.[8][10][24] However, some loose ends remain unresolved.

It is not yet explained why only four HIV groups (HIV-1 groups M and O, and HIV-2 groups A and B) spread considerably in human populations, despite bushmeat practices being widespread in Central and West Africa,[11] and the resulting human SIV infections being common.[24]

It also remains unexplained why all epidemic HIV groups emerged in humans nearly simultaneously, and only in the 20th century, despite very old human exposure to SIV (a recent phylogenetic study demonstrated that SIV is at least tens of thousands of years old).[26]

Origin and epidemic emergence

Several of the theories of HIV origin accept the established knowledge of the HIV/SIV phylogenetic relationships, and also accept that bushmeat practice was the most likely cause of the initial transfer to humans. All of them propose that the simultaneous epidemic emergences of four HIV groups in the late 19th-early 20th century, and the lack of previous known emergences, are explained by new factor(s) that appeared in the relevant African regions in that timeframe. These new factor(s) would have acted either to increase human exposures to SIV, to help it to adapt to the human organism by mutation (thus enhancing its between-humans transmissibility), or to cause an initial burst of transmissions crossing an epidemiological threshold, and therefore increasing the probability of continued spread.

Genetic studies of the virus suggested in 2008 that the most recent common ancestor of the HIV-1 M group dates back to the Belgian Congo city of Léopoldville (modern Kinshasa), circa 1910.[16] Proponents of this dating link the HIV epidemic with the emergence of colonialism and growth of large colonial African cities, leading to social changes, including a higher degree of non-monogamous sexual activity, the spread of prostitution, and the concomitant high frequency of genital ulcer diseases (such as syphilis) in nascent colonial cities.[11]

In 2014, a study conducted by scientists from the University of Oxford and the University of Leuven, in Belgium, revealed that because approximately one million people every year would flow through the prominent city of Kinshasa,[1] which served as the origin of the first known HIV cases in the 1920s,[1] passengers riding on the region's Belgian railway trains were able to spread the virus to larger areas.[1] The study also attributed a roaring sex trade, rapid population growth and unsterilised needles used in health clinics as other factors which contributed to the emergence of the Africa HIV epidemic.[1]

Social changes and urbanization

Beatrice Hahn, Paul M. Sharp, and their colleagues proposed that "[the epidemic emergence of HIV] most likely reflects changes in population structure and behaviour in Africa during the 20th century and perhaps medical interventions that provided the opportunity for rapid human-to-human spread of the virus".[8] After the Scramble for Africa started in the 1880s, European colonial powers established cities, towns, and other colonial stations. A largely masculine labor force was hastily recruited to work in fluvial and sea ports, railways, other infrastructures, and in plantations. This disrupted traditional tribal values and favored casual sexual activity with an increased number of partners. In the nascent cities women felt relatively liberated from rural tribal rules[27] and many remained unmarried or divorced during long periods,[11][28] this being rare in African traditional societies.[29] This was accompanied by unprecedented increase in people's movements.

Michael Worobey and colleagues observed that the growth of cities probably played a role in the epidemic emergence of HIV, since the phylogenetic dating of the two older strains of HIV-1 (groups M and O), suggest that these viruses started to spread soon after the main Central African colonial cities were founded.[16]

Colonialism in Africa

Amit Chitnis, Diana Rawls, and Jim Moore proposed that HIV may have emerged epidemically as a result of the harsh conditions, forced labor, displacement, and unsafe injection and vaccination practices associated with colonialism, particularly in French Equatorial Africa.[30] The workers in plantations, construction projects, and other colonial enterprises were supplied with bushmeat, which would have contributed to an increase in hunting and, it follows, a higher incidence of human exposure to SIV. Several historical sources support the view that bushmeat hunting indeed increased, both because of the necessity to supply workers and because firearms became more widely available.[30][31][32]

The colonial authorities also gave many vaccinations against smallpox, and injections, of which many would be made without sterilising the equipment between uses (unsafe or unsterile injections). Chitnis et al. proposed that both these parenteral risks and the prostitution associated with forced labor camps could have caused serial transmission (or serial passage) of SIV between humans (see discussion of this in the next section).[30] In addition, they proposed that the conditions of extreme stress associated with forced labor could depress the immune system of workers, therefore prolonging the primary acute infection period of someone newly infected by SIV, thus increasing the odds of both adaptation of the virus to humans, and of further transmissions.[33]

The authors proposed that HIV-1 originated in the area of French Equatorial Africa in the early 20th century (when the colonial abuses and forced labor were at their peak). Later researches proved these predictions mostly correct: HIV-1 groups M and O started to spread in humans in late 19th–early 20th century.[13][14][15][16] In addition, all groups of HIV-1 descend from either SIVcpz or SIVgor from apes living to the west of the Ubangi River, either in countries that belonged to the French Equatorial Africa federation of colonies, in Equatorial Guinea (then a Spanish colony), or in Cameroon (which was a German colony between 1884 and 1916, and then fell to Allied forces in World War I, and had most of its area administered by France, in close association with French Equatorial Africa).

This theory was later dubbed "Heart of Darkness" by Jim Moore,[34] alluding to the book of the same title written by Joseph Conrad, the main focus of which is colonial abuses in equatorial Africa.

Unsterile injections

In several articles published since 2001, Preston Marx, Philip Alcabes, and Ernest Drucker proposed that HIV emerged because of rapid serial human-to-human transmission of SIV (after a bushmeat hunter or handler became SIV-infected) through unsafe or unsterile injections.[35][19][36][37] Although both Chitnis et al.[30] and Sharp et al.[8] also suggested that this may have been one of the major risk factors at play in HIV emergence (see above), Marx et al. enunciated the underlying mechanisms in greater detail, and wrote the first review of the injection campaigns made in colonial Africa.[19][36]

Central to Marx et al. argument is the concept of adaptation by serial passage (or serial transmission): an adventitious virus (or other pathogen) can increase its biological adaptation to a new host species if it is rapidly transmitted between hosts, while each host is still in the acute infection period. This process favors the accumulation of adaptive mutations more rapidly, therefore increasing the odds that a better adapted viral variant will appear in the host before the immune system suppresses the virus.[19] Such better adapted variant could then survive in the human host for longer than the short acute infection period, in high numbers (high viral load), which would grant it more possibilities of epidemic spread.

Marx et al. reported experiments of cross-species transfer of SIV in captive monkeys (some of which made by themselves), in which the use of serial passage helped to adapt SIV to the new monkey species after passage by three or four animals.[19]

In agreement with this model is also the fact that, while both HIV-1 and HIV-2 attain substantial viral loads in the human organism, adventitious SIV infecting humans seldom does so: people with SIV antibodies often have very low or even undetectable SIV viral load.[24] This suggests that both HIV-1 and HIV-2 are adapted to humans, and serial passage could have been the process responsible for it.

Marx et al. proposed that unsterile injections (that is, injections where the needle or syringe is reused without sterilization or cleaning between uses), which were likely very prevalent in Africa, during both the colonial period and afterwards, provided the mechanism of serial passage that permitted HIV to adapt to humans, therefore explaining why it emerged epidemically only in the 20th century.[19][36]

Massive injections of the antibiotic era

Marx et al. emphasize the massive number of injections administered in Africa after antibiotics were introduced (around 1950) as being the most likely implicated in the origin of HIV because, by these times (roughly in the period 1950 to 1970), injection intensity in Africa was maximal. They argued that a serial passage chain of 3 or 4 transmissions between humans is an unlikely event (the probability of transmission after a needle reuse is something between 0.3% and 2%, and only a few people have an acute SIV infection at any time), and so HIV emergence may have required the very high frequency of injections of the antibiotic era.[19]

The molecular dating studies place the initial spread of the epidemic HIV groups before that time (see above).[13][14][15][16][20][21] According to Marx et al., these studies could have overestimated the age of the HIV groups, because they depend on a molecular clock assumption, may not have accounted for the effects of natural selection in the viruses, and the serial passage process alone would be associated with strong natural selection.[19]

Injection campaigns against sleeping sickness

David Gisselquist proposed that the mass injection campaigns to treat trypanosomiasis (sleeping sickness) in Central Africa were responsible for the emergence of HIV-1.[38] Unlike Marx et al.,[19] Gisselquist argued that the millions of unsafe injections administered during these campaigns were sufficient to spread rare HIV infections into an epidemic, and that evolution of HIV through serial passage was not essential to the emergence of the HIV epidemic in the 20th century.[38]

This theory focuses on injection campaigns that peaked in the period 1910–40, that is, around the time the HIV-1 groups started to spread.[13][14][15][16] It also focuses on the fact that many of the injections in these campaigns were intravenous (which are more likely to transmit SIV/HIV than subcutaneous or intramuscular injections), and many of the patients received many (often more than 10) injections per year, therefore increasing the odds of SIV serial passage.[38]

Other early injection campaigns

Jacques Pépin and Annie-Claude Labbé reviewed the colonial health reports of Cameroon and French Equatorial Africa for the period 1921–59, calculating the incidences of the diseases requiring intravenous injections. They concluded that trypanosomiasis, leprosy, yaws, and syphilis were responsible for most intravenous injections. Schistosomiasis, tuberculosis, and vaccinations against smallpox represented lower parenteral risks: schistosomiasis cases were relatively few; tuberculosis patients only became numerous after mid-century; and there were few smallpox vaccinations in the lifetime of each person.[39]

The authors suggested that the very high prevalence of the Hepatitis C virus in southern Cameroon and forested areas of French Equatorial Africa (around 40–50%) can be better explained by the unsterile injections used to treat yaws, because this disease was much more prevalent than syphilis, trypanosomiasis, and leprosy in these areas. They suggested that all these parenteral risks caused not only the massive spread of Hepatitis C but also the spread of other pathogens, and the emergence of HIV-1: "the same procedures could have exponentially amplified HIV-1, from a single hunter/cook occupationally infected with SIVcpz to several thousand patients treated with arsenicals or other drugs, a threshold beyond which sexual transmission could prosper."[39] They do not suggest specifically serial passage as the mechanism of adaptation.

According to Pépin's 2011 book, The Origins of AIDS,[40] the virus can be traced to a central African bush hunter in 1921, with colonial medical campaigns using improperly sterilized syringe and needles playing a key role in enabling a future epidemic. Pépin concludes that AIDS spread silently in Africa for decades, fueled by urbanization and prostitution since the initial cross-species infection. Pépin also claims that the virus was brought to the Americas by a Haitian teacher returning home from Zaire in the 1960s.[41] Sex tourism and contaminated blood transfusion centers ultimately propelled AIDS to public consciousness in the 1980s and a worldwide pandemic.[40]

Genital ulcer diseases and evolution of sexual activity

João Dinis de Sousa, Viktor Müller, Philippe Lemey, and Anne-Mieke Vandamme proposed that HIV became epidemic through sexual serial transmission, in nascent colonial cities, helped by a high frequency of genital ulcers, caused by genital ulcer diseases (GUD).[11] GUD are simply sexually transmitted diseases that cause genital ulcers; examples are syphilis, chancroid, lymphogranuloma venereum, and genital herpes. These diseases increase the probability of HIV transmission dramatically, from around 0.01–0.1% to 4–43% per heterosexual act, because the genital ulcers provide a portal of viral entry, and contain many activated T cells expressing the CCR5 co-receptor, the main cell targets of HIV.[11][42]

Probable time interval of cross-species transfer

Sousa et al. use molecular dating techniques to estimate the time when each HIV group split from its closest SIV lineage. Each HIV group necessarily crossed to humans between this time and the time when it started to spread (the time of the MRCA), because after the MRCA certainly all lineages were already in humans, and before the split with the closest simian strain, the lineage was in a simian. HIV-1 groups M and O split from their closest SIVs around 1931 and 1915, respectively. This information, together with the datations of the HIV groups' MRCAs, mean that all HIV groups likely crossed to humans in the early 20th century.[11]

Strong GUD incidence in nascent colonial cities

The authors reviewed colonial medical articles and archived medical reports of the countries at or near the ranges of chimpanzees, gorillas and sooty mangabeys, and found that genital ulcer diseases peaked in the colonial cities during their early growth period (up to 1935). The colonial authorities recruited men to work in railways, fluvial and sea ports, and other infrastructure projects, and most of these men did not bring their wives with them. Then, the highly male-biased sex ratio favoured prostitution, which in its turn caused an explosion of GUD (especially syphilis and chancroid). After the mid-1930s, people's movements were more tightly controlled, and mass surveys and treatments (of arsenicals and other drugs) were organized, and so the GUD incidences started to decline. They declined even further after World War II, because of the heavy use of antibiotics, so that, by the late 1950s, Léopoldville (which is the probable center of HIV-1 group M) had a very low GUD incidence. Similar processes happened in the cities of Cameroon and Ivory Coast, where HIV-1 group O and HIV-2 respectively evolved.[11]

Therefore, the peak GUD incidences in cities[11] have a good temporal coincidence with the period when all main HIV groups crossed to humans and started to spread.[11][13][14][15][16][20][21] In addition, the authors gathered evidence that syphilis and the other GUDs were, like injections, absent from the densely forested areas of Central and West Africa before organized colonialism socially disrupted these areas (starting in the 1880s).[11] Thus, this theory also potentially explains why HIV emerged only after the late 19th century.

Female genital mutilation

Uli Linke has argued that the practice of female genital mutilation is responsible for the high incidence of AIDS in Africa, since intercourse with a circumcised female is conducive to exchange of blood.[43]

Male circumcision distribution and HIV origins

Male circumcision may reduce the probability of HIV acquisition by men. Leaving aside blood transfusions, the highest HIV-1 transmissibility ever measured was from GUD-suffering female prostitutes to uncircumcised men—the measured risk was 43% in a single sexual act.[42] Sousa et al. reasoned that the adaptation and epidemic emergence of each HIV group may have required such extreme conditions, and thus reviewed the existing ethnographic literature for patterns of male circumcision and hunting of apes and monkeys for bushmeat, focusing on the period 1880–1960, and on most of the 318 ethnic groups living in Central and West Africa.[11] They also collected censuses and other literature showing the ethnic composition of colonial cities in this period. Then, they estimated the circumcision frequencies of the Central African cities over time.

Sousa et al. charts reveal that male circumcision frequencies were much lower in several cities of western and central Africa in the early 20th century than they are currently. The reason is that many ethnic groups not performing circumcision by that time gradually adopted it, to imitate other ethnic groups and enhance the social acceptance of their boys (colonialism produced massive intermixing between African ethnic groups).[11][29] About 15–30% of men in Léopoldville and Douala in the early 20th century should be uncircumcised, and these cities were the probable centers of HIV-1 groups M and O, respectively.[11]

The authors studied early circumcision frequencies in 12 cities of Central and West Africa, to test if this variable correlated with HIV emergence. This correlation was strong for HIV-2: among 6 West African cities that could have received immigrants infected with SIVsmm, the two cities from the Ivory Coast studied (Abidjan and Bouaké) had much higher frequency of uncircumcised men (60–85%) than the others, and epidemic HIV-2 groups emerged initially in this country only. This correlation was less clear for HIV-1 in Central Africa.[11]

Computer simulations of HIV emergence

Sousa et al. then built computer simulations to test if an 'ill-adapted SIV' (meaning a simian immunodeficiency virus already infecting a human but incapable of transmission beyond the short acute infection period) could spread in colonial cities. The simulations used parameters of sexual transmission obtained from the current HIV literature. They modelled people's 'sexual links', with different levels of sexual partner change among different categories of people (prostitutes, single women with several partners a year, married women, and men), according to data obtained from modern studies of sexual activity in African cities. The simulations let the parameters (city size, proportion of people married, GUD frequency, male circumcision frequency, and transmission parameters) vary, and explored several scenarios. Each scenario was run 1,000 times, to test the probability of SIV generating long chains of sexual transmission. The authors postulated that such long chains of sexual transmission were necessary for the SIV strain to adapt better to humans, becoming an HIV capable of further epidemic emergence.

The main result was that genital ulcer frequency was by far the most decisive factor. For the GUD levels prevailing in Léopoldville in the early 20th century, long chains of SIV transmission had a high probability. For the lower GUD levels existing in the same city in the late 1950s (see above), they were much less likely. And without GUD (a situation typical of villages in forested equatorial Africa before colonialism) SIV could not spread at all. City size was not an important factor. The authors propose that these findings explain the temporal patterns of HIV emergence: no HIV emerging in tens of thousands of years of human slaughtering of apes and monkeys, several HIV groups emerging in the nascent, GUD-riddled, colonial cities, and no epidemically successful HIV group emerging in mid-20th century, when GUD was more controlled, and cities were much bigger.

Male circumcision had little to moderate effect in their simulations, but, given the geographical correlation found, the authors propose that it could have had an indirect role, either by increasing genital ulcer disease itself (it is known that syphilis, chancroid, and several other GUDs have higher incidences in uncircumcised men), or by permitting further spread of the HIV strain, after the first chains of sexual transmission permitted adaptation to the human organism.

One of the main advantages of this theory is stressed by the authors: "It [the theory] also offers a conceptual simplicity because it proposes as causal factors for SIV adaptation to humans and initial spread the very same factors that most promote the continued spread of HIV nowadays: promiscuous [sic] sex, particularly involving sex workers, GUD, and possibly lack of circumcision."[11]

Iatrogenic and other theories

Iatrogenic theories propose that medical interventions were responsible for HIV origins. By proposing factors that only appeared in Central and West Africa after the late 19th century, they seek to explain why all HIV groups also started after that.

The theories centered on the role of parenteral risks, such as unsterile injections, transfusions,[19][30][38][39] or smallpox vaccinations[30] are accepted as plausible by most scientists of the field.

Discredited HIV/AIDS origins theories include several iatrogenic theories, such as Edward Hooper's 1999 claim that early oral polio vaccines, contaminated with a chimpanzee virus, caused the Central African outbreak.[44]

Pathogenicity of SIV in non-human primates

In most non-human primate species, natural SIV infection does not cause a fatal disease (but see below). Comparison of the gene sequence of SIV with HIV should, therefore, give us information about the factors necessary to cause disease in humans. The factors that determine the virulence of HIV as compared to most SIVs are only now being elucidated. Non-human SIVs contain a nef gene that down-regulates CD3, CD4, and MHC class I expression; most non-human SIVs, therefore, do not induce immunodeficiency; the HIV-1 nef gene, however, has lost its ability to down-regulate CD3, which results in the immune activation and apoptosis that is characteristic of chronic HIV infection.[45]

In addition, a long-term survey of chimpanzees naturally infected with SIVcpz in Gombe, Tanzania found that, contrary to the previous paradigm, chimpanzees with SIVcpz infection do experience an increased mortality, and also suffer from a Human AIDS-like illness.[46] SIV pathogenicity in wild animals could exist in other chimpanzee subspecies and other primate species as well, and stay unrecognized by lack of relevant long term studies.

History of spread

Main article: Timeline of early HIV/AIDS cases

1959: David Carr

David Carr was an apprentice printer (usually referred to, mistakenly, as a sailor; Carr had served in the Navy between 1955 and 1957) from Manchester, England who died August 31, 1959, and was for some time mistakenly reported to have died from AIDS-defining opportunistic infections (ADOIs). Following the failure of his immune system, he succumbed to pneumonia. Doctors, baffled by what he had died from, preserved 50 of his tissue samples for inspection. In 1990, the tissues were found to be HIV-positive. However, in 1992, a second test by AIDS researcher David Ho found that the strain of HIV present in the tissues was similar to those found in 1990 rather than an earlier strain (which would have mutated considerably over the course of 30 years). He concluded that the DNA samples provided actually came from a 1990 AIDS patient. Upon retesting David Carr's tissues, he found no sign of the virus.[47][48][49]

1959: Congolese man

One of the earliest documented HIV-1 infections was discovered in a preserved blood sample taken in 1959 from a man from Léopoldville in the Belgian Congo.[50] However, it is unknown whether this anonymous person ever developed AIDS and died of its complications.[50]

1960: Congolese woman

A second early documented HIV-1 infection was discovered in a preserved lymph node biopsy sample taken in 1960 from a woman from Léopoldville, Belgian Congo.[16]

1969: Robert Rayford

Main article: Robert Rayford

In May 1969 16-year-old African-American Robert Rayford died at the St. Louis City Hospital from Kaposi's sarcoma. In 1987 researchers at Tulane University School of Medicine detected "a virus closely related or identical to"[51] HIV-1 in his preserved blood and tissues. The doctors who worked on his case at the time suspected he was a prostitute or the victim of sexual abuse, though the patient did not discuss his sexual history with them in detail.[51][52][53][54][55]

1969: Arvid Noe

Main article: Arvid Noe

In 1975 and 1976, a Norwegian sailor, with the alias name Arvid Noe, his wife, and his seven-year-old daughter died of AIDS. The sailor had first presented symptoms in 1969, eight years after he first spent time in ports along the West African coastline. A gonorrhea infection during his first African voyage shows he was sexually active at this time. Tissue samples from the sailor and his wife were tested in 1988 and found to contain HIV-1 (Group O).[56][57]

1973: Ugandan children

From 1972 to 1973, researchers drew blood from 75 children in Uganda to serve as controls for a study of Burkitt's lymphoma. In 1985, retroactive testing of the frozen blood serum indicated that antibodies to a virus related to HIV were present in 50 of the children.[58]

Spread to the Western Hemisphere

HIV-1 strains were once thought to have arrived in New York City from Haiti around 1971.[59][60][61] It spread from New York City to San Francisco around 1976.[59]

HIV-1 is believed to have arrived in Haiti from central Africa, possibly from the Democratic Republic of the Congo around 1967.[59][62] The current consensus is that HIV was introduced to Haiti by an unknown individual or individuals who contracted it while working in the Democratic Republic of the Congo circa 1966, or from another person who worked there during that time.[61] A mini-epidemic followed, and, circa 1969, yet another unknown individual took HIV from Haiti to the United States. The vast majority of cases of AIDS outside sub-Saharan Africa can be traced back to that single patient[60] (although numerous unrelated incidents of AIDS among Haitian immigrants to the U.S. were recorded in the early 1980s, and, as evidenced by the case of Robert Rayford, isolated incidents of this infection may have been occurring as early as 1966). The virus eventually entered male gay communities in large United States cities, where a combination of casual, multi-partner sexual activity (with individuals reportedly averaging over 11 unprotected sexual partners per year[63]) and relatively high transmission rates associated with anal intercourse[64] allowed it to spread explosively enough to finally be noticed.[60]

Because of the long incubation period of HIV (up to a decade or longer) before symptoms of AIDS appear, and, because of the initially low incidence, HIV was not noticed at first. By the time the first reported cases of AIDS were found in large United States cities, the prevalence of HIV infection in some communities had passed 5%.[65] Worldwide, HIV infection has spread from urban to rural areas, and has appeared in regions such as China and India.

Canadian flight attendant theory

Main article: Gaëtan Dugas

A Canadian airline steward named Gaëtan Dugas was referred to as "Case 057" and later "Patient O" for "outside Southern California", in an early AIDS study by Dr. William Darrow of the Centers for Disease Control.[59] Because of this, many people had considered Dugas to be responsible for taking HIV to North America. However, HIV had arrived in New York City around 1971 and he did not start work at Air Canada until 1974.[59] In Randy Shilts' 1987 book And the Band Played On (and the 1993 movie based on it, Dugas is referred to as AIDS' Patient Zero instead of "Patient O", but neither the book nor the movie states that he had been the first to bring the virus to North America. He was incorrectly called "Patient Zero" because at least 40 of the 248 people known to be infected by HIV in 1983 had had sex with him, or with someone who had sexual intercourse with him.

1981: From GRID to AIDS

The AIDS epidemic officially began on June 5, 1981, when the U.S. Centers for Disease Control and Prevention in its Morbidity and Mortality Weekly Report newsletter reported unusual clusters of Pneumocystis pneumonia (PCP) caused by a form of Pneumocystis carinii (now recognized as a distinct species Pneumocystis jirovecii) in five homosexual men in Los Angeles.[66]

Over the next 18 months, more PCP clusters were discovered among otherwise healthy men in cities throughout the country, along with other opportunistic diseases (such as Kaposi's sarcoma[67] and persistent, generalized lymphadenopathy[68]), common in immunosuppressed patients.

In June 1982, a report of a group of cases amongst gay men in Southern California suggested that a sexually transmitted infectious agent might be the etiological agent,[69] and the syndrome was initially termed "GRID", or gay-related immune deficiency.[70]

Health authorities soon realized that nearly half of the people identified with the syndrome were not homosexual men. The same opportunistic infections were also reported among hemophiliacs,[71] users of intravenous drugs such as heroin, and Haitian immigrants – leading some researchers to call it the "4H" disease.[72][73]

By August 1982, the disease was being referred to by its new CDC-coined name: Acquired Immune Deficiency Syndrome (AIDS).[74]

Identification of the virus

May 1983: LAV

In May 1983, doctors from Dr. Luc Montagnier's team at the Pasteur Institute in France reported that they had isolated a new retrovirus from lymphoid ganglions that they believed was the cause of AIDS.[75] The virus was later named lymphadenopathy-associated virus (LAV) and a sample was sent to the U.S. Centers for Disease Control, which was later passed to the National Cancer Institute (NCI).[75][76]

May 1984: HTLV-III

In May 1984 a team led by Robert Gallo of the United States confirmed the discovery of the virus, but they renamed it human T lymphotropic virus type III (HTLV-III).[77]

August 1984: ARV

Dr. Jay Levy's group at the University of California, San Francisco also played a role in the discovery of HIV. He independently isolated the AIDS virus in 1983 and named it the AIDS-associated Retrovirus (ARV).[78]

January 1985: both found to be the same

In January 1985, a number of more-detailed reports were published concerning LAV and HTLV-III, and by March it was clear that the viruses were the same, were from the same source, and were the etiological agent of AIDS.[79][80]

May 1986: the name HIV

In May 1986, the International Committee on Taxonomy of Viruses ruled that both names should be dropped and a new name, HIV (Human Immunodeficiency Virus), be used.[81]

Nobel

Whether Gallo or Montagnier deserve more credit for the discovery of the virus that causes AIDS has been a matter of considerable controversy. Together with his colleague Françoise Barré-Sinoussi, Montagnier was awarded one half of the 2008 Nobel Prize in Physiology or Medicine for his "discovery of human immunodeficiency virus".[82] Harald zur Hausen also shared the prize for his discovery that human papilloma virus leads to cervical cancer, but Gallo was left out.[83] Gallo said that it was "a disappointment" that he was not named a co-recipient.[84] Montagnier said he was "surprised" Gallo was not recognized by the Nobel Committee: "It was important to prove that HIV was the cause of AIDS, and Gallo had a very important role in that. I'm very sorry for Robert Gallo."[83] Dr Levy’s contribution to the discovery of HIV was also cited in the Noble Prize ceremony.

Case definition for epidemiological surveillance

Since June 5, 1981, many definitions have been developed for epidemiological surveillance such as the Bangui definition and the 1994 expanded World Health Organization AIDS case definition.

Genetic studies

Further information: Simian immunodeficiency virus § History

According to a study published in the Proceedings of the National Academy of Sciences in 2008, a team led by Robert Shafer at Stanford University School of Medicine has discovered that the gray mouse lemur has an endogenous lentivirus (the genus to which HIV belongs) in its genetic makeup. This suggests that lentiviruses have existed for at least 14 million years, much longer than the currently known existence of HIV. In addition, the time frame falls in the period when Madagascar was still connected to what is now the African continent; the said lemurs later developed immunity to the virus strain and survived an era when the lentivirus was widespread among other mammalia. The study is being hailed as crucial, because it fills the blanks in the origin of the virus, as well as in its evolution, and may be important in the development of new antiviral drugs.[85]

In 2010, researchers reported that SIV had infected monkeys in Bioko for at least 32,000 years. Previous to this time, it was thought that SIV infection in monkeys had happened over the past few hundred years.[86] Scientists estimated that it would take a similar amount of time before humans adapted naturally to HIV infection in the way monkeys in Africa have adapted to SIV and not suffer any harm from the infection.[87]

A 2016 Czech study of the genome of Malayan flying lemurs, an order of mammals parallel to primates and sharing an immediate common ancestor with them, found endogenous lentiviruses that emerged an estimated 40-60 million years ago based on rates of viral mutation versus modern lentiviruses.[88]

Discredited hypotheses

Main article: Discredited AIDS origins theories

Other hypotheses for the origin of AIDS have been proposed. AIDS denialism argues that HIV or AIDS does not exist or that AIDS is not caused by HIV; some of its proponents believe that AIDS is caused by lifestyle, including sexuality or drug use, and not by HIV. Some conspiracy theories allege that HIV was created in a bioweapons laboratory, perhaps as an agent of genocide or an accident. These hypotheses have been rejected by scientific consensus; it is generally accepted among pathologists that "…the evidence that HIV causes AIDS is scientifically conclusive",[89] and most "scientific" arguments for denialism are based on misrepresentations of outdated data.

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"Denying science". Nature Medicine. 12 (4): 369–369. 2006-04-01. doi:10.1038/nm0406-369. ISSN 1078-8956. To support their ideas, some AIDS denialists have also misappropriated a scientific review in Nature Medicine which opens with this reasonable statement: "Despite considerable advances in HIV science in the past 20 years, the reason why HIV-1 infection is pathogenic is still debated."

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