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Typical Sequence of Events in Primary HIV

Event Day

Infection 0

Entry of virus into bloodstream 3-7

Detectable HIV-1 RNA 7-14

Detectable p24 antigen 12-19

Onset of symptoms 14-28

Antibody seroconversion 30-60

1. Bell DM. Am J Med 1997;102(suppl 5B):9--15.

2. Ippolito G et al. Arch Int Med 1993;153:1451--8.

3. Am J Epidemiology 1999;150:306-11.

4. Am J Epidemiology 1999;150:306-11.

5. MMWR 47;RR-17, 1998.

6. NEJM 336(15):1072-8. (rates in Europe & U.S.)

7. Am J Epidemiology 1999;150:306-11.

8. Rothenberg RB et al. AIDS 1998;12:2095-2105.

9. MMWR 47;RR-17, 1998.

10. ACTG 076

1 Course of HIV-1 Disease

During primary infection there is a decline in CD4+ cell count, an increase in the plasma HIV RNA and an increase in the HIV antibodies. During clinical latency, the antibody level begins to fall, the CD4+ cell count is stable. Viral clearance and production of new virions is fairly constant. As the symptoms progress to AIDS the CD4+ cell count decreases, the plasma HIV RNA increases and the HIV antibody concentration decreases.

7% - 5 детей- полная профилактика (1-точно получала со 2 триместра, но свежая ВИЧ-инфекция, 1-лечение начато во 2 триместре, точно получала, ВИЧ-инфекция несвежая)

14,5% - 10 детей – 2+3 ЭТАПЫ (ZDV) (2 женщины начали получать ZDV в 32 и 36 недель, роды на 38 неделе, поэтому не включены в 3-этапную профилактику)

11,5% - 8 детей -2+3 этапы (NVP)

3% - 2 детей – 3 этап

64% - 44 пары мать-ребенок – не получали ХП

Since 1994, the proportion of HIV patients receiving HAART has risen steadily. A corresponding decrease in AIDS and death has been seen.1

1.EuroSIDA November 2000.

The main aims of ART are to reduce viral load, improve immune function and quality of life and, most importantly, to reduce HIV-related morbidity and mortality.

How and why does resistance emerge?–
Competition within the prevailing environment

wThe competitive edge depends on the prevailing environment of the virus; use of one or more suppressive antiretrovirals changes the environment to favour other populations over the wild-type.

wPopulations with even a very small degree of resistance to one or more of the drugs used will quickly seize the bulk of the residual replication under therapy; these so-called ‘escape mutants’ may not cause regimen failure directly, but will provide the ‘backbone’ for further, stepwise accumulation of mutations increasing the degree of resistance to give an eventual outgrowth.

wUse of multiple drugs in a regimen significantly delays the development of resistance in two ways:

•By markedly reducing the likelihood of there being a pre-existing escape mutant in the quasispecies, particularly if more than a single mechanistic class is employed.

•By reducing residual replication by a much greater amount than that derived from only one or two drugs.

wIn principle, a sufficient number of drugs in a regimen might be expected to suppress replication to such a degree that, even were an escape mutant to eventually emerge, it would be functionally disabled and non-reproductive.

wHowever, to date, no combination of drugs has proved to be ‘resistance-proof’ in this way.

•

What is resistance and why is it a concern?

w“HIV drug resistance” describes a loss of HIV susceptibility to the antiviral activity of one or more drugs.

wResistant strains of HIV emerge under antiretroviral therapy and undermine the efficacy of the whole treatment regimen, ultimately resulting in rebound of plasma viraemia.

wDrug resistance is a major cause of regimen failure and restricts the overall duration of effective therapy by steadily eroding the drug options available.

wResistant strains can also be transmitted from one person to another and can therefore restrict the options even in those who have yet to begin treatment.