Identifying HIV infection in diagnostic histopathology tissue samples - the role of HIV-1 p24 immunohistochemistry in identifying clinically unsuspected HIV infection: a 3-year analysis

2010 ◽  
Vol 56 (4) ◽  
pp. 530-541 ◽  
Author(s):  
Mufaddal T Moonim ◽  
Lida Alarcon ◽  
Janet Freeman ◽  
Ula Mahadeva ◽  
Jon D van der Walt ◽  
...  
Keyword(s):  
Hiv Infection ◽  
Tissue Samples ◽  
Hiv 1 ◽  
Diagnostic Histopathology

scholarly journals Structural and Functional Role of INI1, a Cellular Cofactor of HIV-1 integrase in the Early Step of HIV Infection

2011 ◽  
Vol 100 (3) ◽  
pp. 324a
Author(s):  
Benoit Maillot ◽  
Corinne Crucifix ◽  
Sylvia Eiler ◽  
Karine Pradeau ◽  
Nicolas Levy ◽  
...  
Keyword(s):  
Hiv Infection ◽  
Functional Role ◽  
Early Step ◽  
Cellular Cofactor ◽  
Hiv 1

Human Immunodeficiency Virus (HIV)-Resistant CD4+ UT-7 Megakaryocytic Human Cell Line Becomes Highly HIV-1 and HIV-2 Susceptible Upon CXCR4 Transfection: Induction of Cell Differentiation by HIV-1 Infection

Blood ◽  
1997 ◽  
Vol 89 (8) ◽  
pp. 2670-2678 ◽  
Author(s):  
Marta Baiocchi ◽  
Eleonora Olivetta ◽  
Cristiana Chelucci ◽  
Anna Claudia Santarcangelo ◽  
Roberta Bona ◽  
...  
Keyword(s):  
Human Immunodeficiency Virus ◽  
Hiv Infection ◽  
Cell Line ◽  
Viral Entry ◽  
Human Cell Line ◽  
Immunodeficiency Virus ◽  
Hiv Entry ◽  
Stromal Cell Derived Factor ◽  
Hiv 1

Abstract Recent findings have shown that the expression of the seven trans-membrane G-protein–coupled CXCR4 (the receptor for the stromal cell-derived factor [SDF]-1 chemokine) is necessary for the entry of T-lymphotropic human immunodeficiency virus (HIV) strains, acting as a coreceptor of the CD4 molecule. In the human system, the role of CXCR4 in HIV infection has been determined through env-mediated cell fusion assays and confirmed by blocking viral entry in CD4+/CXCR4+ cells by SDF-1 pretreatment. We observed that the human megakaryoblastic CD4+ UT-7 cell line fails to express CXCR4 RNA and is fully resistant to HIV entry. Transfection of an expression vector containing the CXCR4 c-DNA rendered UT-7 cells readily infectable by different T-lymphotropic syncytium-inducing HIV-1 and HIV-2 isolates. Interestingly, HIV-1 infection of CXCR4 expressing UT-7 cells (named UT-7/fus) induces the formation of polynucleated cells through a process highly reminiscent of megakaryocytic differentiation and maturation. On the contrary, no morphologic changes were observed in HIV-2–infected UT-7/fus cells. These findings further strengthen the role of CXCR4 as a molecule necessary for the replication of T-lymphotropic HIV-1 and HIV-2 isolates and provide a useful model to study the functional role of CD4 coreceptors in HIV infection.

scholarly journals DC-SIGN–mediated Infectious Synapse Formation Enhances X4 HIV-1 Transmission from Dendritic Cells to T Cells

2004 ◽  
Vol 200 (10) ◽  
pp. 1279-1288 ◽  
Author(s):  
Jean-François Arrighi ◽  
Marjorie Pion ◽  
Eduardo Garcia ◽  
Jean-Michel Escola ◽  
Yvette van Kooyk ◽  
...  
Keyword(s):  
T Cells ◽  
Dendritic Cells ◽  
T Cell ◽  
Hiv Infection ◽  
Cd4 T Cells ◽  
Synapse Formation ◽  
Model Systems ◽  
Hiv 1 ◽  
Infectious Synapse

Dendritic cells (DCs) are essential for the early events of human immunodeficiency virus (HIV) infection. Model systems of HIV sexual transmission have shown that DCs expressing the DC-specific C-type lectin DC-SIGN capture and internalize HIV at mucosal surfaces and efficiently transfer HIV to CD4+ T cells in lymph nodes, where viral replication occurs. Upon DC–T cell clustering, internalized HIV accumulates on the DC side at the contact zone (infectious synapse), between DCs and T cells, whereas HIV receptors and coreceptors are enriched on the T cell side. Viral concentration at the infectious synapse may explain, at least in part, why DC transmission of HIV to T cells is so efficient. Here, we have investigated the role of DC-SIGN on primary DCs in X4 HIV-1 capture and transmission using small interfering RNA–expressing lentiviral vectors to specifically knockdown DC-SIGN. We demonstrate that DC-SIGN− DCs internalize X4 HIV-1 as well as DC-SIGN+ DCs, although binding of virions is reduced. Strikingly, DC-SIGN knockdown in DCs selectively impairs infectious synapse formation between DCs and resting CD4+ T cells, but does not prevent the formation of DC–T cells conjugates. Our results demonstrate that DC-SIGN is required downstream from viral capture for the formation of the infectious synapse between DCs and T cells. These findings provide a novel explanation for the role of DC-SIGN in the transfer and enhancement of HIV infection from DCs to T cells, a crucial step for HIV transmission and pathogenesis.

Relationships Between HIV-Mediated Chemokine Coreceptor Signaling, Cofilin Hyperactivation, Viral Tropism Switch and HIV-Mediated CD4 Depletion

2020 ◽  
Vol 17 (6) ◽  
pp. 388-396
Author(s):  
Sijia He ◽  
Yuntao Wu
Keyword(s):  
Immune Deficiency ◽  
T Cells ◽  
Virus Infection ◽  
Hiv Infection ◽  
Cd4 T Cells ◽  
Cd4 T Cell ◽  
Viral Tropism ◽  
High Pathogenicity ◽  
Hiv 1

: HIV infection causes CD4 depletion and immune deficiency. The virus infects CD4 T cells through binding to CD4 and one of the chemokine coreceptors, CXCR4 (X4) or CCR5 (R5). It has also been known that HIV tropism switch, from R5 to X4, is associated with rapid CD4 depletion, suggesting a key role of viral factors in driving CD4 depletion. However, the virological driver for HIV-mediated CD4 depletion has not been fully elucidated. We hypothesized that HIV-mediated chemokine coreceptor signaling, particularly chronic signaling through CXCR4, plays a major role in CD4 dysfunction and depletion; we also hypothesized that there is an R5X4 signaling (R5X4sig) viral subspecies, evolving from the natural replication course of R5-utilizing viruses, that is responsible for CD4 T cell depletion in R5 virus infection. To gain traction for our hypothesis, in this review, we discuss a recent finding from Cui and co-authors who described the rapid tropism switch and high pathogenicity of an HIV-1 R5 virus, CRF01_AE. We speculate that CRF01_AE may be the hypothetical R5X4sig viral species that is rapidly evolving towards the X4 phenotype. We also attempt to discuss the intricate relationships between HIV-mediated chemokine coreceptor signaling, viral tropism switch and HIV-mediated CD4 depletion, in hopes of providing a deeper understanding of HIV pathogenesis in blood CD4 T cells.

scholarly journals Inhibition of HIV infection by structural proteins of the inner nuclear membrane is associated with reduced chromatin dynamics

2020 ◽  
Author(s):  
Anvita Bhargava ◽  
Mathieu Maurin ◽  
Patricia M. Davidson ◽  
Mabel Jouve ◽  
Xavier Lahaye ◽  
...  
Keyword(s):  
Dna Damage ◽  
Hiv Infection ◽  
Nuclear Envelope ◽  
Dna Damage Response ◽  
Hela Cells ◽  
Nuclear Pore ◽  
Lamin A ◽  
Damage Response ◽  
Hiv 1

AbstractThe Human Immunodeficiency Virus (HIV) enters the nucleus to establish infection. HIV interacts with nuclear pore components to cross the nuclear envelope. In contrast, the role of other proteins of the nuclear envelope in HIV infection is not yet understood. The inner nuclear transmembrane proteins SUN1 and SUN2 connect lamins in the interior of the nucleus to the cytoskeleton in the cytoplasm. Increased levels of SUN1 or SUN2 potently restrict HIV infection through an unresolved mechanism. Here, we find that SUN1 and SUN2 exhibit a differential and viral strain-specific antiviral activity HIV-1 and HIV-2. In macrophages and HeLa cells, HIV-1 and HIV-2 are respectively preferentially inhibited by SUN1 and SUN2. This specificity maps to the nucleoplasmic domain of SUN proteins, which associates with Lamin A/C and participates to the DNA damage response. We find that etoposide, a DNA-damaging drug, stimulates infection. Inhibition of the DNA damage signaling kinase ATR, which induces a DNA damage response, also enhances HIV-1 infection. The proviral effect of ATR inhibition on infection requires the HIV-1 Vpr gene. Depletion of endogenous Lamin A/C, which sensitizes cells to DNA damage, also enhances HIV-1 infection in HeLa cells. SUN1 overexpression neutralizes these proviral effects, while the antiviral effect of SUN2 is rescued by etoposide treatment. Finally, we show that inhibition of HIV-1 infection by overexpressed SUN proteins and endogenous Lamin A/C is associated with reduced internal movements of chromatin and reduced rotations of the nucleus. Altogether, these results highlight distinct antiviral activities of SUN1 and SUN2 and reveal an emerging role of nuclear movements and the DNA damage response in the control of HIV infection by structural components of the nuclear envelope.

The potential role of the HIV-1 immunogen (Remune®) as a therapeutic vaccine in the treatment of HIV infection

2003 ◽  
Vol 2 (6) ◽  
pp. 739-752 ◽  
Author(s):  
Eduardo Fernandez-Cruz ◽  
Joaquín Navarro ◽  
Carmen Rodriguez-Sainz ◽  
Juana Gil ◽  
Santiago Moreno ◽  
...  
Keyword(s):  
Hiv Infection ◽  
Potential Role ◽  
Therapeutic Vaccine ◽  
Hiv 1

scholarly journals Interactive Effects of Morphine on HIV Infection: Role in HIV-Associated Neurocognitive Disorder

2012 ◽  
Vol 2012 ◽  
pp. 1-10 ◽  
Author(s):  
Pichili Vijaya Bhaskar Reddy ◽  
Sudheesh Pilakka-Kanthikeel ◽  
Shailendra K. Saxena ◽  
Zainulabedin Saiyed ◽  
Madhavan P. N. Nair
Keyword(s):  
Drug Abuse ◽  
Hiv Infection ◽  
Injection Drug Users ◽  
Drug Users ◽  
Public Health Problem ◽  
Mapk Signaling ◽  
Interactive Effects ◽  
Hiv 1 ◽  
Neural Dysfunction

HIV epidemic continues to be a severe public health problem and concern within USA and across the globe with about 33 million people infected with HIV. The frequency of drug abuse among HIV infected patients is rapidly increasing and is another major issue since injection drug users are at a greater risk of developing HIV associated neurocognitive dysfunctions compared to non-drug users infected with HIV. Brain is a major target for many of the recreational drugs and HIV. Evidences suggest that opiate drug abuse is a risk factor in HIV infection, neural dysfunction and progression to AIDS. The information available on the role of morphine as a cofactor in the neuropathogenesis of HIV is scanty. This review summarizes the results that help in understanding the role of morphine use in HIV infection and neural dysfunction. Studies show that morphine enhances HIV-1 infection by suppressing IL-8, downregulating chemokines with reciprocal upregulation of HIV coreceptors. Morphine also activates MAPK signaling and downregulates cAMP response element-binding protein (CREB). Better understanding on the role of morphine in HIV infection and mechanisms through which morphine mediates its effects may help in devising novel therapeutic strategies against HIV-1 infection in opiate using HIV-infected population.

scholarly journals Role of Semen on Vaginal HIV-1 Transmission and Maraviroc Protection

2015 ◽  
Vol 59 (12) ◽  
pp. 7847-7851 ◽  
Author(s):  
Olivia D. Council ◽  
Michael D. Swanson ◽  
Rae Ann Spagnuolo ◽  
Angela Wahl ◽  
J. Victor Garcia
Keyword(s):  
Bone Marrow ◽  
Hiv Infection ◽  
Hiv Transmission ◽  
Humanized Mice ◽  
Vaginal Transmission ◽  
Hiv 1

ABSTRACTWe used bone marrow/liver/thymus (BLT) humanized mice to establish the effect of semen on vaginal HIV infection and on the efficacy of topically applied maraviroc. Our results demonstrate that vaginal transmission of cell-free HIV occurs efficiently in the presence of semen and that topically applied maraviroc efficiently prevents HIV transmission in the presence of semen. We also show that semen has no significant effect on the transmission of transmitted/founder viruses or cell-associated viruses.

scholarly journals Sex Differences in Primary HIV Infection: Revisiting the Role of TLR7-Driven Type 1 IFN Production by Plasmacytoid Dendritic Cells in Women

2021 ◽  
Vol 12 ◽  
Author(s):  
Jean-Charles Guéry
Keyword(s):  
Dendritic Cells ◽  
Hiv Infection ◽  
X Chromosome ◽  
Type I Interferon ◽  
Acute Infection ◽  
Plasmacytoid Dendritic Cells ◽  
Type I ◽  
Hiv 1 ◽  
Tlr7 Stimulation

Plasmacytoid dendritic cells (pDCs) produce type I interferon (IFN-I) during HIV-1 infection in response to TLR7 stimulation. However, IFN-I-signaling has been shown to play opposite effects in HIV-1 and SIV infection. TLR7-driven type I interferon production in pDCs is higher in women than in men due to the cell-intrinsic actions of estrogen and X-chromosome complement. Indeed, TLR7 is encoded on the X-chromosome, and the TLR7 gene escapes the X-chromosome inactivation in immune cells of women which express significantly higher levels of TLR7 protein than male cells. Following HIV infection, women have a lower viremia during acute infection and exhibit stronger antiviral responses than men, which has been attributed to the increased capacity of female pDCs to produce IFN-α upon TLR7-stimulation. However, a deleterious functional impact of an excessive TLR7 response on acute viremia in women has been recently revealed by the analysis of the frequent rs179008 c.32A>T SNP of TLR7. This SNP was identified as a sex-specific protein abundance quantitative trait locus (pQTL) causing a difference in the TLR7 protein dosage and effector function in females only. T allele expression was associated with a lower TLR7 protein synthesis, blunted production of IFN-α by pDCs upon TLR7 stimulation, and an unexpectedly lower viral load during primary HIV-1 infection in women. In the present review, the author will revisit the role of TLR7-driven pDC innate function in the context of HIV-1 infection to discuss at what stage of primary HIV-1 infection the TLR7 rs179008 T allele is likely to be protective in women.

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