HIV-1 transmission worldwide is predominantly associated with heterosexual
activity, and non-clade B viruses account for the most spread. The HIV-1 ep
idemic in Trinidad/Tobago and the Caribbean shares many features with such
heterosexual epidemics, including a prominent role for coincident sexually
transmitted diseases. This study evaluates the molecular epidemiology of HI
V-1 in Trinidad/ Tobago during a period when abrupt transition from homosex
ual to heterosexual transmission occurred in the absence of injecting drug
use, concomitant with a rapid rise in HIV-1 prevalence in the heterosexual
population. Of 31 viral isolates studied during 1987-1995, all cluster with
subtype B reference strains. In the analysis of full env genes from 22 ear
ly seroconverters, the Trinidad isolates constitute a significant subcluste
r within the B subtype, The Trinidad V3 consensus sequence differs by a sin
gle amino acid from the prototype B V3 consensus and demonstrates stability
over the decade of this study. In the majority of isolates, the Vs loop of
env contains a signature threonine deletion that marks the lineage of the
Trinidad HIV-I clade B epidemic from pre-1984. No phenotypic features, incl
uding syncitium induction, neutralization profiles, and chemokine receptor
usage, distinguish this virus population from other subtype a viruses. Thus
, although the subtype B HIV-1 viruses being transmitted in Trinidad are ge
netically distinguishable from other subtype B viruses, this is probably th
e result of a strong founder effect in a geographically circumscribed popul
ation rather than genetic selection for heterosexual transmission. These re
sults demonstrate that canonical clade B HIV-1 can generate a typical heter
osexual epidemic.