Human Immunodeficiency Virus (HIV)

,

doi:10.1159/000445852

Cited by 248 publications

(120 citation statements)

References 182 publications

(235 reference statements)

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“…The potential functions of exosomes secreted during HIV-1 and HIV-2 infections are just beginning to be explored. HIV-1 and HIV-2 share the same modes of transmission [ 63 ]. Immunodeficiency develops gradually in people that are infected with HIV-2.…”

Section: Human Immunodeficiency Virusmentioning

confidence: 99%

Exosome Biogenesis and Biological Function in Response to Viral Infections

Crenshaw

Sims

et al. 2018

TOVJ

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Introduction:Exosomes are extracellular vesicles that originate as intraluminal vesicles during the process of multivescular body formation. Exosomes mediate intercellular transfer of functional proteins, lipids, and RNAs. The investigation into the formation and role of exosomes in viral infections is still being elucidated. Exosomes and several viruses share similar structural and molecular characteristics.Explanation:It has been documented that viral hijacking exploits the exosomal pathway and mimics cellular protein trafficking. Exosomes released from virus-infected cells contain a variety of viral and host cellular factors that are able to modify recipient host cell responses. Recent studies have demonstrated that exosomes are crucial components in the pathogenesis of virus infection. Exosomes also allow the host to produce effective immunity against pathogens by activating antiviral mechanisms and transporting antiviral factors between adjacent cells.Conclusion:Given the ever-growing roles and importance of exosomes in both host and pathogen response, this review will address the impact role of exosome biogenesis and composition after DNA, RNA virus, on Retrovirus infections. This review also will also address how exosomes can be used as therapeutic agents as well as a vaccine vehicles.

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Section: Human Immunodeficiency Virusmentioning

confidence: 99%

Exosome Biogenesis and Biological Function in Response to Viral Infections

Crenshaw

Sims

et al. 2018

TOVJ

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“…Beneath the surface membrane is p17, a matrix protein that is encoded by the gag gene. This gene also encodes the core proteins p24 and p6 and the nucleocapsid protein p7 which is bound to viral RNA [21,22].…”

Section: Human Immunodeficiency Virusmentioning

confidence: 99%

“…Other proteins such as Tat, promote transcription, while Rev is responsible for the transport of messenger RNA from the nucleus to the cytoplasm. Vpr, another protein, ensures that the reverse transcribed DNA is able to access the nucleus of non-dividing cells, while signal transduction and the down-regulation of the CD4 antigen, in order to allow the budding process to take place, is facilitated by the viral protein known as Nef [21,22].…”

Section: Human Immunodeficiency Virusmentioning

confidence: 99%

Do Blood Group Antigens and the Red Cell Membrane Influence Human Immunodeficiency Virus Infection?

Davison

Hendrickse

Matsha

2020

Cells

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The expression of blood group antigens varies across human populations and geographical regions due to natural selection and the influence of environment factors and disease. The red cell membrane is host to numerous surface antigens which are able to influence susceptibility to disease, by acting as receptors for pathogens, or by influencing the immune response. Investigations have shown that Human Immunodeficiency Virus (HIV) can bind and gain entry into erythrocytes, and therefore it is hypothesized that blood groups could play a role in this process. The ABO blood group has been well studied. However, its role in HIV susceptibility remains controversial, while other blood group antigens, and the secretor status of individuals, have been implicated. The Duffy antigen is a chemokine receptor that is important in the inflammatory response. Those who lack this antigen, and type as Duffy null, could therefore be susceptible to HIV infection, especially if associated with neutropenia. Other antigens including those in the Rh, Lutheran and OK blood group systems have all been shown to interact with HIV. More recently, experiments show that cells which overexpress the Pk antigen appear to be protected against infection. These reports all demonstrate that red cell antigens interact and influence HIV infection. However, as the red cell membrane is complex and the pathogenesis of HIV multi-factorial, the role of blood group antigens cannot be studied in isolation.

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“…The structural proteins included the group-specific antigen (p55 gag polyprotein), a polyprotein which is processed by viral proteases during maturation to matrix protein (p17), capsid protein (p24), spacer peptide 1 (p2), nucleocapsid protein (p7), spacer peptide 2 (p1), and P6 protein. Other structural proteins involve the polymerase (Pol) and the envelope protein (gp160) that is post-translationally processed to produce the surface glycoprotein (gp120) and gp41 that mediate binding to the CD4 receptor, and envelope fusion to target cells, respectively ( 28 ).…”

Section: Microbiota Contribution In Hiv Interaction With Bonementioning

confidence: 99%

Influence of HIV Infection and Antiretroviral Therapy on Bone Homeostasis

Delpino

Quarleri

2020

Front. Endocrinol.

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The human immunodeficiency virus type 1 (HIV)/AIDS pandemic represents the most significant global health challenge in modern history. This infection leads toward an inflammatory state associated with chronic immune dysregulation activation that tilts the immune-skeletal interface and its deep integration between cell types and cytokines with a strong influence on skeletal renewal and exacerbated bone loss. Hence, reduced bone mineral density is a complication among HIV–infected individuals that may progress to osteoporosis, thus increasing their prevalence of fractures. Highly active antiretroviral therapy (HAART) can effectively control HIV replication but the regimens, that include tenofovir disoproxil fumarate (TDF), may accelerate bone mass density loss. Molecular mechanisms of HIV-associated bone disease include the OPG/RANKL/RANK system dysregulation. Thereby, osteoclastogenesis and osteolytic activity are promoted after the osteoclast precursor infection, accompanied by a deleterious effect on osteoblast and its precursor cells, with exacerbated senescence of mesenchymal stem cells (MSCs). This review summarizes recent basic research data on HIV pathogenesis and its relation to bone quality. It also sheds light on HAART-related detrimental effects on bone metabolism, providing a better understanding of the molecular mechanisms involved in bone dysfunction and damage as well as how the HIV-associated imbalance on the gut microbiome may contribute to bone disease.

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Human Immunodeficiency Virus (HIV)

Cited by 248 publications

References 182 publications

Exosome Biogenesis and Biological Function in Response to Viral Infections

Exosome Biogenesis and Biological Function in Response to Viral Infections

Do Blood Group Antigens and the Red Cell Membrane Influence Human Immunodeficiency Virus Infection?

Influence of HIV Infection and Antiretroviral Therapy on Bone Homeostasis

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