Similar HIV-1 evolution and immunological responses at 10 years despite several therapeutic strategies and host HLA Types.
Two sexual partners infected with related HIV-1 viruses and enrolled in different therapeutic strategies including structured treatment interruptions (STI) provided us an opportunity to compare long term (10 years) viral genetic evolution for closely related isolates in different hosts. HLA loci were molecularly typed and different genetic markers were studied. The viral genetic evolution was studied by sequencing pol and env genes. The HIV-specific CD4+ and CD8+ T cell responses were assessed by the lymphoproliferative response (LPR) and an ELISPOT assay, respectively. HLA class I loci of patients A and B were different and both of them were heterozygous for CCR5delta32 gene. During the two STI studies, viral load of both patients rebounded after treatment interruption and both developed a transitory strong helper and CTL responses. After definitive interruption of therapy, viral load remained below 5,000 copies/ml without therapy during the two years of follow-up. Two patients infected with related viruses showed a similar dynamics of viral evolution and CD4 T cells, despite hosts having a different HLA type and being treated with several therapeutic protocols, after 10 years of infection. These results suggest that, in this case, an effective immunological response to STI depended more on the virus than on the characteristics of the host.
Arnedo-Valero
Mireia
M
Microbiology, Hospital Clínic, Faculty of Medicine, University of Barcelona, Barcelona, Spain. arnedo@medicina.ub.es
Plana
Montserrat
M
Mas
Antonio
A
Guilà
Meritxell
M
Gil
Cristina
C
Castro
Pedro
P
Garcia
Felipe
F
Domingo
Esteban
E
Gatell
Josep Ma
JM
Pumarola
Tomàs
T
D019380:Anti-HIV Agents / Q000627:therapeutic use; D018791:CD4 Lymphocyte Count; D004334:Drug Administration Schedule; D004359:Drug Therapy, Combination; D019143:Evolution, Molecular; D005260:Female; D015658:HIV Infections / Q000188:drug therapy* / Q000276:immunology* / Q000821:virology; D015497:HIV-1 / Q000235:genetics* / Q000276:immunology; D020010:Heterosexuality; D006650:Histocompatibility Testing; D006801:Humans; D008297:Male; D008969:Molecular Sequence Data; D019713:Receptors, CCR5 / Q000235:genetics; D018894:Reverse Transcriptase Inhibitors / Q000627:therapeutic use; D012747:Sexual Partners; D013602:T-Lymphocytes, Cytotoxic; D013997:Time Factors; D019562:Viral Load
D019380:Anti-HIV Agents; D019713:Receptors, CCR5; D018894:Reverse Transcriptase Inhibitors