scholarly journals Anti-Gag antibodies gag HIV infection and slow disease progression

AIDS ◽  
2018 ◽  
Vol 32 (10) ◽  
pp. 1373-1375 ◽  
Author(s):  
Ali Ahmad ◽  
Vikram Mehraj ◽  
Mohammad-Ali Jenabian ◽  
Jean-Pierre Routy ◽  
Cecile Tremblay

2010 ◽  
Vol 2 (2) ◽  
pp. 18 ◽  
Author(s):  
Stefano Di Bella ◽  
Elisabetta Grilli ◽  
Maria Adriana Cataldo ◽  
Nicola Petrosillo

Selenium is a non-metallic chemical element of great important to human health. Low selenium levels in humans are associated with several pathological conditions and are a common finding in HIV infected individuals. We conducted a review of the literature to assess if selenium deficiency or selenium supplementation could play a role in modifying the clinical course of HIV disease. Several studies investigated the role of selenium in disease progression, morbidity and mortality in HIV infected individuals. Larger studies were conducted in countries with poor economic resources and limited access to HAART. According to the majority of published studies low selenium levels appear to have an association with mortality, and selenium supplementation appears to play a beneficial role on survival or on slowing disease progression among HIV infected individuals. The role of selenium supplementation on preventing hospital admission among HIV outpatients was also noticed. The literature suggests an association between selenium deficiency and development of HIV associated cardiomyopathy and furthermore, selenium supplementation appears to improve the cardiac function in HIV infected individuals with cardiomyopathy. However, there is conflicting evidence regarding the role selenium in modifying HIV viral load and immune status in HIV infection.



2022 ◽  
Vol 14 (1) ◽  
Author(s):  
Boghuma K. Titanji ◽  
Marta Gwinn ◽  
Vincent C. Marconi ◽  
Yan V. Sun

AbstractDespite significant advances in the treatment and care of people with HIV (PWH), several challenges remain in our understanding of disease pathogenesis to improve patient care. HIV infection can modify the host epigenome and as such can impact disease progression, as well as the molecular processes driving non-AIDS comorbidities in PWH. Epigenetic epidemiologic studies including epigenome-wide association studies (EWAS) offer a unique set of tools to expand our understanding of HIV disease and to identify novel strategies applicable to treatment and diagnosis in this patient population. In this review, we summarize the current state of knowledge from epigenetic epidemiologic studies of PWH, identify the main challenges of this approach, and highlight future directions for the field. Emerging epigenetic epidemiologic studies of PWH can expand our understanding of HIV infection and health outcomes, improve scientific validity through collaboration and replication, and increase the coverage of diverse populations affected by the global HIV pandemic. Through this review, we hope to highlight the potential of EWAS as a tool for HIV research and to engage more investigators to explore its application to important research questions.



2021 ◽  
Author(s):  
Zhiqiang Zhu ◽  
Qi Liang ◽  
Taiyi Jiang ◽  
Yanmei Jiao ◽  
Yu Zhang

Abstract The date about the condition of HBV co infection with the disease progress of HIV is limited. To investigate whether the incidence of HBV co-infection is significantly higher in HIV patients with disease progression in China, we compared rates of HBV co-infection in HIV patients based on an acute and a chronic HIV infected cohort. Significance was assessed with Chi-square. HBV infection is diagnosed by the presence of hepatitis B surface antigen. The HBsAg positive rate increased from 6.18% in acute HIV infection to 11.44% in chronic HIV infection. Thirty-four acute HIV patients had been tested for HBV in their chronic phase, four of them had HBV -specific antigens and/or specific antibodies changes. The number of Hepatitis B virus-specific antibodies decreased from acute phase to chronic phase in four patients and two patients’ HBsAg changed from negative to positive. There is an increased prevalence of HBV infection in HIV patients with the disease progression in China.



2019 ◽  
Vol 17 (1) ◽  
Author(s):  
Xiaowan Yin ◽  
Zhuo Wang ◽  
Tong Wu ◽  
Meichen Ma ◽  
Zining Zhang ◽  
...  

Abstract Background Chemokines are small chemotactic cytokines involved in inflammation, cell migration, and immune regulation in both physiological and pathological contexts. Here, we investigated the profile of chemokines during primary HIV infection (PHI). Methods Fifty-four participants with blood samples before and during HIV infection and clinical information available were selected from an HIV-negative man who have sex with men (MSM) prospective cohort. Thirty chemokines and 10 cytokines were measured pre- and post-HIV infection in the same individuals using a Bio-Plex Pro™ Human Chemokine Panel. Results Levels of 18 chemokines/cytokines changed significantly during PHI relative to pre-HIV infection levels; 14 were up-regulated and 4 down-regulated. Among them, CXCL9, CXCL10, and CXCL11 were the most prominently raised. Levels of CXCL9 and CXCL10 were much higher in the high-set point group (log viral load (lgVL) ≥ 4.5) than those in the low-set point group (lgVL < 4.5) and levels of CXCL9, CXCL10, and CXCL11 were higher in the low-CD4+ T-cell count group (CD4+ T-cell count ≥ 500). A formula to predict HIV disease progression using a combination panel comprising CXCL9, CXCL10, and CXCL11 was developed, where risk score = 0.007 × CXCL9 + 0.004 × CXCL10 − 0.033 × CXCL11 − 1.724, with risk score values higher than the cutoff threshold (0.5211) indicating more rapid HIV disease progression. Conclusions A panel of plasma CXCL9, CXCL10, and CXCL11 measured during primary HIV-1 infection could predict long-term HIV disease prognosis in an MSM group and has potential as a novel biomarker in the clinic.



2018 ◽  
Vol 92 (13) ◽  
Author(s):  
Diana C. DeLucia ◽  
Charles R. Rinaldo ◽  
Giovanna Rappocciolo

ABSTRACT Professional antigen-presenting cells (APC; myeloid dendritic cells [DC] and macrophages [MΦ]; B lymphocytes) mediate highly efficient HIV-1 infection of CD4 + T cells, termed trans infection, that could contribute to HIV-1 pathogenesis. We have previously shown that lower cholesterol content in DC and B lymphocytes is associated with a lack of HIV-1 trans infection in HIV-1-infected nonprogressors (NP). Here, we assessed whether HIV-1 trans infection mediated by another major APC, MΦ, is deficient in NP due to altered cholesterol metabolism. When comparing healthy HIV-1 seronegatives (SN), rapid progressors (PR), and NP, we found that monocyte-derived MΦ from NP did not mediate HIV-1 trans infection of autologous CD4 + T cells, in contrast to efficient trans infection mediated by SN and PR MΦ. MΦ trans infection efficiency was directly associated with the number of DC-specific intercellular adhesion molecule-3-grabbing nonintegrin (DC-SIGN)-expressing MΦ. Significantly fewer NP MΦ expressed DC-SIGN. Unesterified (free) cholesterol in MΦ cell membranes and lipid rafting was significantly lower in NP than PR, as was virus internalization in early endosomes. Furthermore, simvastatin (SIMV) decreased the subpopulation of DC-SIGN + MΦ as well as cis and trans infection. Notably, SIMV decreased cell membrane cholesterol and led to lipid raft dissociation, effectively mimicking the incompetent APC trans infection environment characteristic of NP. Our data support that DC-SIGN and membrane cholesterol are central to MΦ trans infection, and a lack of these limits HIV-1 disease progression. Targeting the ability of MΦ to drive HIV-1 dissemination in trans could enhance HIV-1 therapeutic strategies. IMPORTANCE Despite the success of combination antiretroviral therapy, neither a vaccine nor a cure for HIV infection has been developed, demonstrating a need for novel prophylactic and therapeutic strategies. Here, we show that efficiency of MΦ-mediated HIV trans infection of CD4 + T cells is a unique characteristic associated with control of disease progression, and it is impaired in HIV-infected NP. In vitro treatment of MΦ from healthy donors with SIMV lowers their cholesterol content, which results in a strongly reduced trans infection ability, similar to the levels of MΦ from NP. Taken together, our data support the hypothesis that MΦ-mediated HIV-1 trans infection plays a role in HIV infection and disease progression and demonstrate that the use of SIMV to decrease this mechanism of virus transfer should be considered for future HIV therapeutic development.





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