R. Bravo et al., VIREMIA QUANTIFICATION IN PATIENTS WITH T HE HUMAN-IMMUNODEFICIENCY-VIRUS WITH RAPID AND SLOW DISEASE PROGRESSION, Medicina Clinica, 104(14), 1995, pp. 530-534
BACKGROUND: The natural course of the human immunodeficiency virus typ
e 1 (HIV-1) infection is very variable. The factors which appear to de
termine the speed of immunodeficiency progression are multiple, althou
gh the virulence of the predominant vial strain seems to be one the ma
in factors. The plasmatic viremia in individuals with rapid and slow H
IV-1 progression was analyzed in an attempt to establish the degree of
correlation between HIV-1 replication and the natural course of the d
isease. METHODS: Forty-two samples from 34 seropositive patients, 11 w
ith rapid progression criteria (< 5 years from acute infection and CD4
+ lymphocytes < 0.2 x 10(9)/l) and 23 with slow progression (> 7 years
from demonstrated infection and > 0.5 x 10(9) CD4+ lymphocytes/l) wer
e studied. The plasmatic viremia was quantified by a new method of pla
sma DNA genetic amplification, denominated the branched DNA (bDNA) tec
hnique. As a reference circulating p24 was determined and the presence
of several proviral regions were studied in peripheral blood lymphocy
tes by polymerase chain reaction (PCR). RESULTS: The presence of RNA m
olecules was detected in plasma of 7 (58.3%) out of 12 samples of rapi
d progression (RP) patients by bDNA. To the contrary, this was negativ
e in 30 samples from slow progression (SP) patients. Four of the 5 neg
ative RP samples corresponded to patients who had taken antiretroviral
drugs at the time of the study. The p24 antigenemia was positive in 5
(41.6%) from the RP patients and in none of the SP patients. The pres
ence of gag, pol and env sequences was positive by PCR in all RP patie
nts and in most of the SP patients. However, repeatedly negative resul
ts by PCR were observed in 5 SP samples for all or some of the genomic
regions studied. CONCLUSIONS: Patients with rapid progression of HIV-
1 have higher plasmatic viremia than subjects with slow disease progre
ssion.