R. Grunow et al., INHIBITION OF SYNCYTIA-INDUCING (SI) VIRUS BY AUTOLOGOUS SERUM FROM HIV-1-INFECTED INDIVIDUALS, Clinical and diagnostic virology, 6(2-3), 1996, pp. 127-135
Background: Progression from HIV infection to AIDS is often accompanie
d or even predicted by a switch of the virus to a more pathogenic or s
yncytia-inducing (SI) phenotype concomitant with the development of HI
V variants escaping neutralizing antibodies. Objective: Here we studie
d the capacity of sera to neutralize autologous SI-HIV or the laborato
ry strain III, and compared these data to the viral load in HIV-l-infe
cted patients. Methods: The SI phenotype of HIV was detected by co-cul
tivation of peripheral blood mononuclear cells (PBMCs) with MT2 cells
in 112 patients stratified by their CD4 cell counts. Sera at dilutions
of 1:15 and 1:75 were added to MT2 co-cultures with autologous PBMCs
as well as with HIV-1/IIIB-infected H9 cells to study the inhibitory c
apacity. The p24 antigenemia was detected by enzyme-linked immunosorbe
nt assay (ELISA) and the circulating HIV RNA was determined using the
polymerase chain reaction (PCR). Results: The SI virus was detected in
PBMCs from 31/65 patients with less than or equal to 200 CD4+ cells,
8/28 patients with 201-499 CD4(+) cells, and 1/19 patients with greate
r than or equal to 500 CD4(+) cells. Sera from 16/40 patients inhibite
d the autologous SI-HIV. In sera from patients with less than or equal
to 200 CD4(+) cells, p24 antigen could be detected in 17/34 (50%) pat
ients with non-syncytia-inducing (NSI) phenotype and in 7/19 (37%) pat
ients carrying SI-HIV without serum inhibition. In contrast, all 12 se
ra with inhibitory activity to the autologous SI-HIV were negative for
p24 antigen. A similar tendency was seen in patients with higher CD4(
+) T-cell counts. The mean load of circulating HIV RNA did not differ
among groups of patients. Independently of their neutralizing activity
to the autologous SI virus, the majority of sera were able to neutral
ize the laboratory HIV-1/IIIB. Conclusions: While most of the patients
' sera neutralized the laboratory HIV-1/IIIB strain, only some sera we
re able to inhibit the autologous SI-HIV. In these cases, the detectab
le SI-HIV may still be controlled by the immune system in vivo, which
is consistent with a low p24 antigenemia.