Search

Increasing evidence has suggested that HIV infection severely damages the Vγ2Vδ2 (Vδ2) T cells that play an important role in the first-line host response to infectious disease. However, little is known about Vδ2 T cell-mediated antibody-dependent cell-mediated cytotoxicity (ADCC) in HIV disease. We found that although the CD16(+) Vδ2 T cell subset hardly participated in phosphoantigen responses dominated by the CD16(-) Vδ2 T cell subset, the potency of the ADCC function of Vδ2 T cells was correlated with the frequency of the CD16(+) subset. Thus, two distinct and complementary Vδ2 T cell subsets discriminated by CD16 were characterized to explore the respective impacts of HIV-1 infection on them. HIV-1 disease progression was not only associated with the phosphoantigen responsiveness of the CD16(-) Vδ2 subset, but also with the ability of the CD16(+) Vδ2 subset to kill antibody-coated target cells. Furthermore, both of the two Vδ2 functional subsets could be partially restored in HIV-infected patients with antiretroviral therapy. Notably, in the context of an overall HIV-mediated Vδ2 T cell depletion, despite the decline of phosphoantigen-responsive CD16(-) Vδ2 cells, CD16(+) Vδ2 cell-mediated ADCC was not compromised but exhibited a functional switch with dramatic promotion of degranulation in the early phase of HIV infection and chronic infection with slower disease progression. Our study reveals functional characterizations of the two Vδ2 T cell subsets with different activation pathways during HIV-1 infection and provides a rational direction for activating the CD16(+) Vδ2 T cells capable of mediating ADCC as a means to control HIV-1 disease.

HIV-1 is capable of mimicking the ligand of integrin α(4)β(7) by displaying a tripeptide mimotope on the V2 region. Through this mimicry HIV can bind the α(4)β(7) integrin and get carried through the lymphocyte proliferation signaling pathway, cell-to-cell adhesion and can migrate to gut-associated lymphoid tissues. The same tripeptide motif was suggested to be the epicenter of neutralization in laboratory strains of HIV-1. In this study, we compared the α(4)β(7) binding sites of two HIV-1 subtypes prevalent in China and found that the tripeptide binding domain of α(4)β(7) was more diverse in subtype B' strains than in CRF07_BC.

HIV-1 CRF07_BC is one of the predominant strains in China, however, there have been few reports about the genetic characteristics of accessory genes of this strain. In this study, 236 CRF07_BC tat exon-1 regions were obtained by nested PCR and were followed by sequencing. Our results showed some variations in crucial functional domains, especially in the basic region. There were two conserved amino acid variations in the 1 approximately 56 aa fragment of tat gene exon-1 of 07_BC isolates, which were R7N (71.6%) and R46F (90.3%), as compared with subtype B' strains in Thailand. The analysis of the sequences provides some valuable information for an exploration of the predominance of the HIV-1 CRF07_BC epidemic.

We report here a novel HIV-1 circulating recombinant form (CRF59_01B), isolated from three epidemiologically unlinked men who have sex with men (MSM) in China. CRF59_01B was composed of subtype CRF01_AE and B, with four identical recombinant breakpoints observed in the pol, env genes and between the 3' tat (or rev) and vpu genes. The emergence of CRF59_01B suggests the increasing significance of homosexual transmission in China's HIV epidemic and may indicate an active transmission network of HIV infections among MSM population in China. Further studies of the molecular epidemiology of HIV-1 epidemic among MSM population in China are necessary to gain a fuller understanding of the transmission network and potential public health impact of HIV -1 among MSM population in this region.