AEGiS-12IAC: HIV-1 subtype D infection in Brazil: molecular identification and clinical and immunological evaluation.

12th International AIDS Conference

Geneva, Switzerland - June 28-July 3, 1998

HIV-1 subtype D infection in Brazil: molecular identification and clinical and immunological evaluation.

Int Conf AIDS 1998 Jun 28-Jul 3; 12:20-1 (abstract no. 11192)

Morgado M, Guimaraes ML, Neves Junior I, Campos-Mello DL, Grinsztejn B, Linhares-de-Carvalho MI, Bongertz V
IOC, FIOCRUZ, Rio De Janeiro, Brazil.

OBJECTIVES: To survey HIV diversity in Brazil and try to evaluate the potential implications of HIV-1 infection with non-B subtypes in the immunological, clinical and virological correlates to progression.

METHODOLOGY: HIV-1 infected individuals were recruited from January 1993 to December 1996 from several cohorts in Rio de Janeiro, Brazil. HIV-1 subtyping has been done by PCR and HMA (Delwart et al. 1993, Science, 262:1257-1261). PCR amplified products of the gp 120 C2-V3 region were sequenced by the dideoxy termination method. T cell subsets were determined by flow cytometry (XL, Coulter Co). Lymphoproliferative response (LPR) to mitogens (PHA and PWM) and antigens (HIV-1 and PPD) were measured by the 3H-Thymidine incorporation. Viral load was determined by NASBA (Organon Teknika).

RESULTS: From the 131 HIV-1 positive individuals analyzed, 106 (80.9%) could be typed as infected by subtype B and 20 (15.3%) by subtype F. One of the samples (0.8%) was classified as subtype D, based on the DNA profile and confirmed by DNA sequencing. This case of subtype D infection was transmitted in Brazil and shows a rapid progressor profile. This individual was diagnosed as HIV-1 seropositive in September, 1996, after having been assumed as seronegative until the beginning of 1995, however, the CD4+ counts were very low (96/mm³) at this first visit, as well as the LPR to PHA. Upon antiRetroviral therapy (AZT and DDI) CD4+ counts varied from 290/mm³ to 81/mm³ whereas plasmatic viral load varied from 30,000 to 130,000 copies/ml. Triple treatment (3TC, D4T and Ritonavir) was introduced and CD4+ counts raised to 278/mm³. During this time, LPR to mitogens and PPD were positive but lower than in the normal controls, and high percentages of activated CD8+/CD38+ Tcell subset (30-45%) were still observed. No positively charged amino acids at the positions 11 or 25 of the gp 120 V3 loop, currently associated with SI virus pattern, were verified in three distinct samples obtained along one year of follow-up.

CONCLUSIONS: The frequency of subtype D infection in Rio de Janeiro City identified so far is still very low, however, preliminary data showed that the only patient identified showed a clinical and immunological profile typical for the rapid progressors. HIV-1 positive patients infected with F and B subtypes are under evaluation. The follow-up of cohorts infected with distinct HIV-1 subtypes in Brazil may represent an important field to evaluate the implications of this diversity for pathogenicity and response to antiRetroviral therapy.

Keywords: AEGIS, HIV Infections, HIV-1, CD4 Lymphocyte Count, Viral Load, HIV Seropositivity, Polymerase Chain Reaction, Brazil, Greece, Human, immunology, ICA12
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