Recent studies of HIV RNA in infected individuals show that viral levels va
ry widely between individuals and within the same individual over time. Ind
ividuals with higher viral loads during the chronic phase tend to develop A
IDS more rapidly. If RNA levels are correlated with infectiousness, these v
ariations explain puzzling results from HIV transmission studies and sugges
t that a small subset of infected people may be responsible for a dispropor
tionate number of infections. We use two simple models to study the impact
of variations in infectiousness. In the first model, we account for differe
nt levels of virus between individuals during the chronic phase of infectio
n, and the increase in the average time from infection to AIDS that goes al
ong with a decreased viral load, The second model follows the more standard
hypothesis that infected individuals progress through a series of infectio
n stages, with the infectiousness of a person depending upon his current di
sease stage. We derive and compare threshold conditions for the two models
and find explicit formulas of their endemic equilibria. We show that formul
as for both models can be put into a standard form, which allows for a clea
r interpretation. We define the relative impact of each group as the fracti
on of infections being caused by that group.We use these formulas and numer
ical simulations to examine the relative importance of different stages of
infection and different chronic levels of virus to the spreading of the dis
ease. The acute stage and the most infectious group both appear to have a d
isproportionate effect, especially on the early epidemic. Contact tracing t
o identify super-spreaders and alertness to the symptoms of acute HIV infec
tion may both be needed to contain this epidemic. (C) 1999 Published by Els
evier Science Inc. All rights reserved.