Catalogo Articoli (Spogli Riviste)

OPAC HELP

Titolo:
INHIBITION OF SYNCYTIA-INDUCING (SI) VIRUS BY AUTOLOGOUS SERUM FROM HIV-1-INFECTED INDIVIDUALS
Autore:
GRUNOW R; VONOVERBECK J; FRUTIG K; FREI E; GERMANN D; FURRER H; PERRIN L; PICHLER WJ;
Indirizzi:
UNIV BERN,INSELSPITAL,INST IMMUNOL & ALLERGOL CH-3010 BERN SWITZERLAND UNIV BERN,INSELSPITAL,INST CLIN IMMUNOL CH-3010 BERN SWITZERLAND UNIV BERN,INSELSPITAL,MED POLICLIN CH-3010 BERN SWITZERLAND UNIV BERN,INSELSPITAL,INST MED MICROBIOL CH-3010 BERN SWITZERLAND HOP CANTONAL UNIV GENEVA,CENT LAB VIROL GENEVA SWITZERLAND
Titolo Testata:
Clinical and diagnostic virology
fascicolo: 2-3, volume: 6, anno: 1996,
pagine: 127 - 135
SICI:
0928-0197(1996)6:2-3<127:IOS(VB>2.0.ZU;2-O
Fonte:
ISI
Lingua:
ENG
Soggetto:
HUMAN-IMMUNODEFICIENCY-VIRUS; HIV-1 BIOLOGICAL PHENOTYPE; DISEASE PROGRESSION; TYPE-1 INFECTION; MONOCLONAL-ANTIBODIES; CD4+ LYMPHOCYTES; VARIABLE DOMAIN; VIRAL PHENOTYPE; PATHOGENESIS; ZIDOVUDINE;
Keywords:
HIV-1; SYNCYTIA FORMATION; NEUTRALIZING ANTIBODIES; VIRAL LOAD;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Science Citation Index Expanded
Citazioni:
38
Recensione:
Indirizzi per estratti:
Citazione:
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

Abstract

Background: Progression from HIV infection to AIDS is often accompanied or even predicted by a switch of the virus to a more pathogenic or syncytia-inducing (SI) phenotype concomitant with the development of HIV variants escaping neutralizing antibodies. Objective: Here we studied the capacity of sera to neutralize autologous SI-HIV or the laboratory strain III, and compared these data to the viral load in HIV-l-infected patients. Methods: The SI phenotype of HIV was detected by co-cultivation of peripheral blood mononuclear cells (PBMCs) with MT2 cellsin 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 PBMCsas well as with HIV-1/IIIB-infected H9 cells to study the inhibitory capacity. The p24 antigenemia was detected by enzyme-linked immunosorbent assay (ELISA) and the circulating HIV RNA was determined using thepolymerase 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 greater than or equal to 500 CD4(+) cells. Sera from 16/40 patients inhibited 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%) patients with non-syncytia-inducing (NSI) phenotype and in 7/19 (37%) patients carrying SI-HIV without serum inhibition. In contrast, all 12 sera 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 differamong groups of patients. Independently of their neutralizing activity to the autologous SI virus, the majority of sera were able to neutralize the laboratory HIV-1/IIIB. Conclusions: While most of the patients' sera neutralized the laboratory HIV-1/IIIB strain, only some sera were able to inhibit the autologous SI-HIV. In these cases, the detectable SI-HIV may still be controlled by the immune system in vivo, whichis consistent with a low p24 antigenemia.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 27/11/20 alle ore 16:13:09