REMEMBER 1981? Reagan became America's oldest president; Egyptian President Anwar as-Sadat was assassinated; Britain's future king tied the knot with Lady Di; Israel annexed the Golan Heights; PW Botha called an early election and was returned to power with a reduced majority.
In Atlanta, Georgia, a handful of victims of an immunity disorder were dying from a range of rare infections. The disorder came to be known as Aids (acquired immune deficiency syndrome). By November last year, 74 countries reported cases of Aids, with more than 25 000 victims in the USA, over 3 000 in Europe and thousands, perhaps hundreds of thousands of unrecognized cases in Africa.
Of the millions more believed to have been infected with the causative virus, as many as a third will develop full-blown Aids by 1997. There is no cure, and no sector of the population is completely safe. Even optimistic scientists doubt that a workable vaccine will become available before the middle of the 1990s. Aids itself does not kill; it strips the body of its defences against disease.
The tricky part has been finding out exactly how the Aids virus -Human Immunodeficiency Virus (HIV) — brings the natural immune system to a grinding halt. The picture, complicated to- the scientists involved, is thousands of times worse for the layperson to understand. It has not been made easier by the different acronyms used by different institutions to describe the same thing.
The confusion started in 1983, when Professor Luc Montagnier and a group of scientists at the Institut Pasteur in Paris isolated the virus responsible, and called it LAV (lymphadenopathy associated virus). Sometime in the same year, a group led by Robert Gallo at the National Cancer Institute independently identified the causative virus, calling it HTLV-III (human T-lymphotropic virus type III). Exactly who found it first is the subject of an ongoing court case in America. The winner will claim patenting rights to the royalties worth millions of dollars on blood tests which use the isolated virus.
At a recent meeting of international virologists, it was agreed that the virus HTLV/LAV should be known as HIV. HIV is a retrovirus — a rare kind of virus with a unique method of reproduction. Remember how genes work: a gene is a piece of deoxyribonucleic acid (DNA) on which is "written" a code for making a protein. This code is transcribed first into a working copy of a similar material, ribonucleic acid (RNA), then into a protein. Many viruses work by insinuating their own genes into the genetic code of animal cell and so passing them off as animal genes. The instructions encoded in these genes tell the cell to make more viruses.
A retrovirus's genes are made of RNA and cannot therefore, get into the genetic code. But HIV makes an enzyme called reverse transcriptase which can make a DNA version to stitch into the cell's DNA. An infected cell will then reproduce the virus. Whilst most retroviruses infect a range of cells, HIV seems to only attack T4 lymphocytes — the so called officers of the immune army.
T4 cells have a vital contribution to make to the body's defensive system. When a foreign molecule is "spotted" inside the body, the T4 cells help in four ways: they influence other T-cells to destroy the aliens by disrupting their cell membrane; they secrete interleukin-2, which bolsters the body's natural killer cells; they secrete gamma-interferon, which stimulates macro-phages to engulf and degrade the virus; and, lastly, they allow B cells (another row in the line of defence) to secrete antibodies particular to the invading antigens.
All this activity is bad news for a virus in the wrong place at the wrong time. But they don't just float there and take it; they have their own counter strategy. Some viruses pretend to be something else; the immune system is fooled and produces inappropriate antibodies to try to fight it. Others wait for an antibody to be sent out to fight, and then change form so that the antibodies will not recognise the newly mutated virus.
The Aids virus is less subtle but fatally effective; it wipes out the immune system before being attacked itself. It does this not by rupturing, the T4 cell's membrane (the tactic many viruses use) but apparently by altering and slowing down the growth of T4 cells, so that in time, only those cells infected with the latent virus are left. In a healthy person, T4 cells make up 60- 80 percent of the circulating T-cell population; in Aids patients they can become too rare to be detected. But how does the virus choose T4 cells to the exclusion of others?
Recent work at London's Institute for Cancer Research and the Institut Pasteur suggests that a region of the cell membrane associated with the T4 marker (the protein that distinguishes the T4 cell from any other) acts as a receptor for the virus, a bit like a landing strip from which the virus disembarks and attacks the cell. But the depletion of T4 cells cannot account for the complete collapse of the immune system in the early stages of the disease, for example, victims may have a normal T4 cell count, and still have weakened immunity systems. It is thought that the virus somehow stimulates infected cells to produce something called soluble suppressor factor, which inhibits certain immune responses.
There is some disagreement as to how exactly it is produced. The virus also makes the surviving T4 cells incapable of the first line of defence in an immune response — recognising the enemy. Briefly, for a T4 cell to home in on its specific antigen (foreign molecule), the receptor located on the surface of the cell must recognise both the antigen and a specific type of protein (Class II MHC) for the T-cell response to be triggered. The virus might interfere with this finely balanced mechanism, either by instructing the infected cells to disrupt the receptor mechanism on its surface, or by reducing the amount of Class II MHC, vital to the successful recognition of the antigen.
At a conference held in Paris in 1986, the world's virologists working with HIV reported that the virus is more devious than anyone had anticipated. It enters the body inside an infected cell, avoiding the new host's antibody defence. Like flu, it can vary its genetic code, and like the common cold, it conceals part of its protein coat which a vaccine could attack. Once it instructs the body's infected cells to replicate the virus, the trans-activator gene boosts production.
Condoms for the cadres — the ANC's way to keep Aids out of South Africa
ONLY 63 cases of full-blown Aids have been reported in South Africa so far, according to statistics reported to the World Health Organisation (WHO) by local medical authorities, and a half again that many have died of the disease. The national Aids Advisory Group of the Department of Health and Population Development gives the present doubling time of the disease as six months. This means we are set to follow the same path of Human Immunodeficiency Virus (HIV) infection that took the US from around 500 cases in 1982 to over 25 000 in 1986.
Apartheid has created excellent conditions for an explosion of Aids cases. Large-scale population mobility, interlinked with civil and regional wars, is the major factor. There are three groups involved; refugees, contract workers and soldiers on both sides. Apartheid has generated two million refugees in Southern Africa, including those who struggle against it, according to War on Want, an international aid agency. The figure, drawn from UN High Commission on Refugees information, is incomplete as it leaves out displaced persons.
Refugees flee SADF actions or the actions of Unita in Angola or Renamo in Mozambique. Zambia and Malawi, both countries with a high mV incidence, are also the countries with the highest numbers of such refugees. A large Lusaka-based survey of blood donors found 17 percent of the blood tested there to be seropositive, or infected with the virus. The Mozambican information agency AIM reports that 70 000 refugees will be repatriated from Malawi, where WHO Aids figures are tenfold higher than in their home country. Some may carry the virus.
The migrant labour system is another apartheid factor which could promote the spread of the virus — contract workers living in all-male hostels. Unprotected sexual contact between carriers and other men or with prostitutes will rapidly spread the virus. As an example: in 1981, eight percent of the prostitutes in Nairobi tested were antibody positive. The current incidence is more than 65 percent. Closer to home, the SA Institute of Medical Research and the Chamber of Mines claim a one in 25 Prevalence of HIV carriers among Malawian mineworkers.
Infected contract workers returning to their families in the rural areas can carry the virus with them. Around two million South Africans leave their families every year in this way. Any serious Aids prevention campaign must militate against the continuation of the migrant labour system; for in countries with a high urban Aids incidence, such as Zambia, the settled rural population shows a negligible level of seropositivity. Soldiers form a third large mobile group. ANC soldiers are trained in some of the Central African countries with the highest Aids incidence.
The ANC's national executive committee last month resolved its personnel would receive HIV screening before entering — and after leaving — South Africa. And in order to institute safer sex practices, tens of thousands of condoms have been ordered. Meanwhile, Archbishop Desmond Tutu spoke out in March about rapes committed by soldiers in Namibia and in South Africa. The Aids virus will be forced upon women otherwise not at risk. But mobility and the brutality of war are not the only factors which can created a large-scale epidemic here.
The latent HIV virus is triggered to induce the lethal syndrome by cofactors, such as stress or malnutrition. As the body's immune system is worn down, secondary epidemics of other endemic diseases, such as tuberculosis and gastro-enteritis, follow. The prevalence of the Aids virus in a population may go unnoticed, being masked by these diseases of poverty. And these poverty-linked diseases are themselves reaching extraordinary proportions in some areas. The south-western Cape last year faced an unexplained 23 percent increase in tuberculosis cases, from 1985.
In Central Africa a shift is occurring in the death pattern, away from the elderly and children and towards men and women in their twenties and thirties. This is both the most sexually active and the most sexually active and the most economically productive group. The economic future of high incidence areas is bleak. If muscle power is relied upon in food production, famine may follow in later years. An entire generation could be lost.
Aids experts throughout the region have charged that the South African government is failing to deal with the issue — in effect, wishing it away. No comprehensive information campaign such as those launched in Europe and the US have seen the light of day here. The global strategy to combat the Aids pandemic is coordinated by the WHO. After help is requested, WHO assesses the official commitment to fighting Aids in a sustained national education and prevention programme. Such WHO programmes are incorporated into the primary health care structures of the nations found to be acceptable. But the non-integrated homeland system and the lack of a national health service could be obstacles to an application made by the South African government, as well as to any serious independent Aids prevention or containment strategy. — Jonathan Shopley and David Bellamy, London
Don't die of ignorance — or of paranoia, either
People cannot, as far as scientists know, contract the virus from mosquitoes. There has been much shock-horror talk of transmission by insects, especially mosquitoes, because their proboscis dips into a pool of blood in much the same way as do re-used needles. The rumours were fuelled by the discovery that the virus can be carried by bedbugs for up to one hour after the bugs had gorged on virus-infected blood.
There is very little need to panic, for three reasons. Firstly, because a carrier's blood has very few infected HIV cells, the chances that the small amount of blood sucked by a mosquito includes an infected cell is minimal. Secondly, the hepatitis B virus, which is more readily parentally transmitted, is not transmitted by anthropods. Thirdly, while children in Kinshasha are vulnerable to insect-borne malaria, very few of them have the Aids virus. This makes it highly unlikely that the virus is spread on the wing. South Africa has escaped lightly — so far. Only an estimated 34 people have died from Aids and a further 63 have been infected. No cases have been reported of black South Africans with the disease.
Professor Barry Schoub, Director of the National Institute for Virology, warns that South Africans should not be complacent. "The Aids virus spreads slowly epidemiologically. Unlike flu, it cannot be passed from one carrier to another easily. But it is slowly making its way southwards through Africa; we will know about it soon enough." Although general Aids research has been conducted at various South African universities for over a year, it was only in January this year that the Medical Research Council established a unit at the Institute to focus on the virus itself.
Funding has been promised for five years, and the virologists staffing the unit have been seconded from other projects within the Institute. The government has not pledged vast sums to stem the virus's imminent spread in this country, and there appear to be no plans for an all-out awareness drive to familiarise and warn people about the disease. "I only. wish there were," says Schoub, "although education is by no means a panacea.
A recent market research poll in Britain has shown that, the large awareness campaign there has failed to a certain extent, and there is a feeling it was a waste of money. The multi-million pound publicity campaign in Britain has tried to highlight the main groups at risk and advise the public how to minimise their chances of catching the virus. "Don't Die of Ignorance" has been their catch-phrase. The message? Cut out sexual promiscuity (the more sexual partners a person has, the more likely they are to find someone with the virus) and always use condoms. — Megan Jones
A DIY diagnosis for that deadly disease
FOR those countries without sophisticated diagnostic laboratories, the World Health Organisation has outlined the following do-it-yourself aid. As a predictive tool, it is thought to be only 60 percent accurate. An adult could have Aids if he or she displays at least two of the major signs plus at least one of the minor signs. In fact, anyone displaying these symptoms for more than a month should be seeking medical advice in any case. The guide should be ignored if the adult already has an immuno-suppression complaint, such as cancer or, severe malnutrition.
MAJOR SIGNS:
- Weight loss of more than 10 percent of body weight
- Chronic diarrhoea for more than one month
- Prolonged fever for more than one month (intermittent or constant)
MINOR SIGNS
- Persistent cough for more than one month
- Generalised pruritic inflammation of the skin
- Recurrent shingles
- Oropharyngeal candidiasis
- Chronic progressive and disseminated herpes simplex infection
- Generalised lymphadenopathy
If the adult has Kaposi's sarcoma (a rare skin cancer) or cryptococcal meningitis, he or she could have Aids without exhibiting any of the above major or minor signs. For a child to have Aids, he or she must present at least two of the major signs with at least two of the minor signs:
MAJOR SIGNS:
- Weight loss or abnormally slow growth
- Chronic diarrhea for more than one month
- Prolonged fever for more than one month
MINOR SIGNS:
- Generalised lymphadenopathy
- Opharyngeal candidiasis
- Repeated common infections (otitis, pharyngitis, etc)
- Persistent cough for more than one month
- Generalised dermatitis (inflammation of the skin)
- Confirmed HIV infection of the mother