HIV and AIDS: A primer
© R.J.Walters 2003. All rights reserved
Definition of AIDS (Acquired ImmunoDeficiency Syndrome):
The presence of antibodies to the Human Immunodeficiency Virus (HIV) associated with a fall in the number of CD4+ T-lymphocytes and the appearance of indicator diseases that are otherwise rarely encountered.
Transmission:
Blood transfusions; sharing infected needles; homosexual and heterosexual intercourse; infected mother to child.
WHAT IS HIV ?
WHAT IS ITS MECHANISM OF ACTION ?
WHICH TARGET CELLS DOES HIV INFECT ?
HOW DOES HIV DEVASTATE THE IMMUNE SYSTEM ?
WHAT STRATEGIES DO WE HAVE TO DEFEND OURSELVES ?
HOW WIDESPREAD IS THE PROBLEM ?
WHAT ARE THE CONSEQUENCES FOR OUR SOCIETY ?
WHAT IS HIV ?
HIV is the name given to a closely related family of `retroviruses' that cause a profound immune dysfunction over time.
Most now believe that HIV infection alone is the primary cause of AIDS.
All retroviruses share a common structure and means of reproduction, although HIV is unique in killing its host cell.
HIV primarily affects cells that express the CD4 `co-receptor' protein:
(1) T4
-lymphocytes (`helper cells' from Thymus)
(2) Monocytes and macrophages
(Antigen-presenting `scavenger' cells)
(3) Dendritic cells
(Antigen-presenting `sentinels')
THEORIES OF HOW HIV CAUSES AIDS
Not mutually exclusive!
HIV directly causes CD4 bearing helper T-cells to malfunction and die.
T-helper cells are thrown off balance by HIV: too many antibodies too few killer cells.
HIV infects dendritic cells, the sentinels of the immune system.
HIV `outwits' and `overwhelms' the immune system through rapid mutation.
HIV causes the immune system to attack itself.
HIV infection triggers T-cell suicide.
HOW CAN WE DEFEND OURSELVES ?
Design drugs to interfere with viral reproduction by inhibiting viral proteins:
e.g. reverse transcriptase - AZT (azidothymdine)
tat
(speeds up transcription) - Ro 31-8959
Vaccination with viral coat proteins (antigens) or disabled virus to block infection.
Vaccination with CD4 molecules to prevent viral entry into cell.
Use hormonal changes to alter `helper' T-cell balance, enhancing `killer' T-cell function:
e.g. monoclonal antibodies against interleukin-4 enhances killer T-cell function.
oral alpha-interferon reduces infections and increases number of T-cells.
Change behaviour: fewer sexual partners - protected sexual intercourse.
WHAT ARE THE CONSEQUENCES FOR OUR SOCIETY ?
100,000 diagnosed AIDS cases in Western Europe by the end of 1992.
19.5 million HIV infections worldwide in 1992, nearly all will develop AIDS.
As many as 120 million HIV infections by 2000 A.D.; explosion predicted in Asia.
Epidemic in Thailand `exponential' with casual sex, prostitution and drug use common; and Uganda where 80% of deaths in 13-44 age group in rural areas are due to AIDS and 20% of adults and 80% of prostitutes in Kampala are infected with HIV.
Should we give AZT and other drugs to sufferers irrespective of cost or effectiveness?
What about the underdeveloped world? $3 billion might halve infections by 2000 A.D..
ECONOMIC COST: Assuming that AZT is not given and only half of AIDS patients receive health care AIDS will cost South African economy £9 billion by 2000 A.D..
Does the pharmaceutical industry have an unhealthy profit motive in AIDS?
In Islamic North Africa and Middle East around 75,000 are infected with HIV; compared to 8 million in sub-Saharan Africa; is AIDS a disease of decadence ?
IS THEIR INNATE RESISTANCE TO HIV IN THE POPULATION ?
Whilst 1% of the US population bears two copies of the delta 32 mutation which confers resistance to HIV infection,
other resistance mutations may exist
Genetic diversity last line of species defence against parasitic infection through high mutation rates, recombination events
and polymorphisms
Ensures sufficient individual variation to prevent complete devastation of population
High price for resistance through genetic variation is the incidence of inherited diseases such as Cystic Fibrosis, Thalassaemia and Sickle-cell anaemia.
Does not prevent need for development of vaccine