T(H)-17 cells have been shown to play a role in bacterial defense, acute inflammation, and autoimmunity. We examined the role of interleukin 17 (IL-17) production in human immunodeficiency virus type 1 (HIV-1) infection. Both HIV-1- and cytomegalovirus (CMV)-specific IL-17-producing CD4(+) T cells were detectable in early HIV-1 infection but were reduced to nondetectable levels in chronic and nonprogressive HIV-1 infection. IL-17-producing CMV-specific cells were not detected in blood from HIV-1-uninfected normal volunteers. Virus-specific T(H)-17 cells could coexpress other cytokines and could express CCR4 or CXCR3. Although the etiology of these cells has yet to be established, we propose that microbial translocation may induce them.
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http://dx.doi.org/10.1128/JVI.02550-07 | DOI Listing |
AIDS Res Hum Retroviruses
January 2025
Clinical Laboratory, The People's Hospital of Baoding, Baoding, China.
Many new circulating recombinant forms (CRFs) and unique recombinant forms (URFs) of human immunodeficiency virus type-1 (HIV-1) have been discovered in populations with multiple circulating HIV-1 genotypes. In this study, we report two novel URFs derived from two HIV-1-positive individuals in Hebei, China, who were infected through homosexual (BDD142) and heterosexual (BDD154) contact. Phylogenetic and recombinant analyses of the two NFLG revealed that they are second-generation recombinant strains originating from the CRF01_AE cluster 4/B and CRF01_AE cluster 5/B strains.
View Article and Find Full Text PDFPLoS Pathog
January 2025
Division of Microbiology and Immunology, Department of Pathology, University of Utah School of Medicine, Salt Lake City, Utah, United States of America.
Retroviruses can be detected by the innate immune sensor cyclic GMP-AMP synthase (cGAS), which recognizes reverse-transcribed DNA and activates an antiviral response. However, the extent to which HIV-1 shields its genome from cGAS recognition remains unclear. To study this process in mechanistic detail, we reconstituted reverse transcription, genome release, and innate immune sensing of HIV-1 in a cell-free system.
View Article and Find Full Text PDFJ Infect Dis
January 2025
Gilead Sciences, Inc., 333 Lakeside Dr., Foster City, CA, 94404 USA.
Background: Lenacapavir is a highly potent first-in-class inhibitor of HIV-1 capsid approved for the treatment of heavily treatment-experienced (HTE) people with HIV-1 (PWH) harboring multidrug resistant (MDR) virus, in combination with an optimized background regimen (OBR). Resistance analyses conducted after 2 years of lenacapavir treatment in the phase 2/3 CAPELLA study are described.
Methods: CAPELLA enrolled viremic HTE PWH with resistance to 2 or more drugs per class in at least 3 of the 4 main drug classes.
Front Immunol
January 2025
Department of Microbiology and Immunology, Geisel School of Medicine at Dartmouth, Lebanon, NH, United States.
Epidemiological evidence suggests that post-menopausal women are more susceptible to HIV infection following sexual intercourse than are younger cohorts for reasons that remain unclear. Here, we evaluated how menopause-associated changes in CD4 T cell numbers and subsets as well as HIV coreceptor expression, particularly CCR5, in the endometrium (EM), endocervix (CX), and ectocervix (ECX) may alter HIV infection susceptibility. Using a tissue-specific mixed cell infection model, we demonstrate that while no changes in CD14 macrophage infection susceptibility were observed, CD4 T cell HIV-1 infection frequency increases following menopause in the EM, but not CX nor ECX.
View Article and Find Full Text PDFPLoS Pathog
January 2025
Division of Infectious Diseases, University of Colorado Anschutz Medical Campus School of Medicine, Aurora, Colorado, United States of America.
Lenacapavir (LEN) is a highly potent, long-acting antiretroviral medication for treating people infected with muti-drug-resistant HIV-1 phenotypes. The inhibitor targets multifaceted functions of the viral capsid protein (CA) during HIV-1 replication. Previous studies have mainly focused on elucidating LEN's mode of action during viral ingress.
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