Spontaneous and antigen-induced chemokine production in exposed but uninfected partners of HIV type 1-infected individuals in North India.
Exposure to human immunodeficiency virus (HIV)-1 does not inevitably result in infection and resistance to HIV-1 infection is observed in different categories of at-risk individuals. In this study, the role of beta-chemokines and alpha-chemokine in providing resistance to HIV-1 infection was evaluated in a group of 25 HIV-exposed but uninfected (EU) partners of HIV-1-infected individuals. We studied the levels of regulated on activation, normal T expressed and secreted (RANTES), macrophage inflammatory protein (MIP)-1 alpha, MIP-1 beta , and stromal cell-derived factor (SDF)-1alpha in culture supernatants of peripheral blood mononuclear cells (PBMCs) after stimulation with HIV gag p24 antigen and phytohemagglutinin (PHA). Higher gag-specific beta-chemokine responses were seen in EU individuals and HIV-positive controls when compared with healthy controls (HC). No significant difference was observed in PHA-specific beta-chemokine production between these three groups. Moreover, a spontaneous production of all the three beta-chemokines by unstimulated PBMCs was observed in EU individuals and HIV-positive controls. No significant difference was observed in alpha-chemokine (SDF-1) levels between the three groups after p24 and PHA stimulation. We conclude that in our cohort of EU individuals, beta-chemokines-mediated resistance against HIV might be present. Since beta-chemokines are produced mainly by activated T cells, our results suggest that enhanced chemokine production might be due to exposure to HIV in these individuals.
Suresh
P
P
Department of Internal Medicine, Post Graduate Institute of Medical Education and Research, Chandigarh 160012, India.
Wanchu
Ajay
A
Bhatnagar
Archana
A
Sachdeva
Ravinder Kaur
RK
Sharma
Meera
M
D000328:Adult; D000956:Antigens, Viral; D016022:Case-Control Studies; D054405:Chemokine CCL3; D054407:Chemokine CCL4; D018946:Chemokine CCL5 / Q000378:metabolism*; D054377:Chemokine CXCL12; D019742:Chemokines, CC / Q000378:metabolism*; D019743:Chemokines, CXC / Q000378:metabolism*; D005260:Female; D016655:HIV Core Protein p24; D015658:HIV Infections / Q000097:blood* / Q000276:immunology / Q000517:prevention & control; D018023:HIV Seronegativity / Q000276:immunology* / Q000502:physiology; D015497:HIV-1 / Q000276:immunology*; D006801:Humans; D007113:Immunity, Innate; D007963:Leukocytes, Mononuclear / Q000276:immunology* / Q000821:virology; D008297:Male; D008875:Middle Aged; D010835:Phytohemagglutinins; D013601:T-Lymphocytes / Q000378:metabolism
D000956:Antigens, Viral; C515429:CCL3 protein, human; C066507:CCL4 protein, human; C515255:CXCL12 protein, human; D054405:Chemokine CCL3; D054407:Chemokine CCL4; D018946:Chemokine CCL5; D054377:Chemokine CXCL12; D019742:Chemokines, CC; D019743:Chemokines, CXC; D016655:HIV Core Protein p24; D010835:Phytohemagglutinins