Nef enhances HIV-1 replication and infectivity independently of SERINC5 in CEM T cells

Ramirez, Peter W; Vollbrecht, Thomas; Acosta, Francisco M.; Suarez, Marissa; Angerstein, Aaron O.; Wallace, Jared; Connell, Ryan M O'

doi:10.1016/j.virol.2022.12.008

Cited by 2 publications

(2 citation statements)

References 70 publications

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“…Several observations from patient cohorts and different natural hosts of lentivirus infection also suggest a crucial role for S5: the magnitude by which lentiviral Nefs can antagonize S5 correlates with the prevalence of the corresponding lentiviral lineage [ 19 ]; correlations were reported for the extent of S5 antagonism with clinical progression and viral load [ 38 , 39 , 40 , 41 ], and levels of SERINC mRNA have been found to be decreased in HIV patients [ 42 ]. On the other hand, Nef can boost HIV-1 replication in the absence of SERINC proteins in some cell systems [ 43 , 44 ], and an SIV Nef variant that potently targets human S5 for degradation does not facilitate HIV-1 spread in primary human CD4 T cells [ 45 ]. While these partially contradictory findings imply that the antiviral activities of SERINC proteins depend on the cellular context, a confounding problem in this field remains that the detection of SERINC proteins expressed at endogenous levels is difficult, and physiological protein expression distribution and levels remain unknown.…”

Section: Expression and Role Of Serinc Proteins In Hiv Pathogenesismentioning

confidence: 99%

Beyond Impairment of Virion Infectivity: New Activities of the Anti-HIV Host Cell Factor SERINC5

Sid Ahmed,

Bajak,

Fackler

2024

Viruses

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Members of the serine incorporator (SERINC) protein family exert broad antiviral activity, and many viruses encode SERINC antagonists to circumvent these restrictions. Significant new insight was recently gained into the mechanisms that mediate restriction and antagonism. In this review, we summarize our current understanding of the mode of action and relevance of SERINC proteins in HIV-1 infection. Particular focus will be placed on recent findings that provided important new mechanistic insights into the restriction of HIV-1 virion infectivity, including the discovery of SERINC’s lipid scramblase activity and its antagonism by the HIV-1 pathogenesis factor Nef. We also discuss the identification and implications of several additional antiviral activities by which SERINC proteins enhance pro-inflammatory signaling and reduce viral gene expression in myeloid cells. SERINC proteins emerge as versatile and multifunctional regulators of cell-intrinsic immunity against HIV-1 infection.

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Section: Expression and Role Of Serinc Proteins In Hiv Pathogenesismentioning

confidence: 99%

Beyond Impairment of Virion Infectivity: New Activities of the Anti-HIV Host Cell Factor SERINC5

Sid Ahmed,

Bajak,

Fackler

2024

Viruses

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“…Some viral proteins, such as Tat, Nef, Vpr, and glycoprotein 120 (gp120), are involved in indirect HIV effects, such as elevation of pro-inflammatory cytokines and oxidative stress [29,30]. In particular, Tat, which controls HIV transcription, is able to induce not only oxidative stress [reactive oxygen species (ROS) generation, lipid peroxidation], but also the expression of vascular cell adhesion molecule (VCAM)-1 and intercellular adhesion molecule 1 (ICAM-1), as well as to lower antioxidants (e.g., glutathione-GSH) [30][31][32][33][34]. With regards to Nef protein, it increases superoxide release, also by decreasing endothelial nitric oxide (NO) synthase (eNOS) expression and NO release [25,[35][36][37], while Vpr protein promotes cell-cycle arrest, induces DNA damage and apoptosis, and modulates nuclear factor-kappa B (NF-κB) activity; Vpr is also able to reactivate viral production in latently infected cells by releasing ROS and the pro-inflammatory cytokine IL-6 [38][39][40].…”

Section: Hivmentioning

confidence: 99%

Viral infections in cardiometabolic risk and disease between old acquaintances and new enemies

Vassalle

2023

Explor Cardiol

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Atherosclerosis is a chronic disease, characterized by chronic inflammation, endothelial dysfunction, and lipid deposition in the vessel. Although many major, well-identified risk factors for atherosclerosis [e.g., hyperlipidemia, hypertension, type 2 diabetes (T2D), smoking habit, and obesity] explain a lot about the risk, there is a considerable number of patients who develop atherosclerotic damage and undergo adverse events without presenting any of these established modifiable risk factors. This observation has stimulated an urgent need to expand knowledge towards the identification of additional, less established risk factors that may help in the assessment of risk and fill the gap of knowledge in the cardiovascular (CV) setting. Among them, the hypothesis of a possible relationship between viral infectious agents and atherosclerosis has risen since the early 1900s. However, there is still a great deal of debate regarding the onset and progression of CV disease in relation to the roles of the pathogens (as active inducers or bystanders), host genomic counterparts, and environmental triggers, affecting both virus abundance and the composition of viral communities. Accordingly, the aim of this review is to discuss the current state of knowledge on infectious agents in the atherosclerotic process, with particular focus on two environmental-related viruses, as examples of familiar (influenza) and unfamiliar [severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2)] disease triggers.

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Nef enhances HIV-1 replication and infectivity independently of SERINC5 in CEM T cells

Cited by 2 publications

References 70 publications

Beyond Impairment of Virion Infectivity: New Activities of the Anti-HIV Host Cell Factor SERINC5

Beyond Impairment of Virion Infectivity: New Activities of the Anti-HIV Host Cell Factor SERINC5

Viral infections in cardiometabolic risk and disease between old acquaintances and new enemies

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