Comparative Analysis of Virology and Pathogenesis of SARS-CoV-2 and HIV Infections: Implications for Public Health and Treatment Strategies

Infection and Drug Resistance, Journal Year: 2025, Volume and Issue: Volume 18, P. 269 - 283

Published: Jan. 1, 2025

Introduction: Coronavirus Disease 19 (COVID-19), caused by the Severe Acute Respiratory Syndrome 2 (SARS-CoV -2), and Human Immunodeficiency Virus (HIV) are significant 21st-century pandemics with distinct virological clinical characteristics.COVID-19 primarily presents as an acute respiratory illness, while HIV leads to chronic immune suppression.Understanding their differences can enhance public health strategies treatment approaches.Purpose: This narrative review compares virology, transmission, responses, outcomes of SARS-CoV-2 inform interventions.Methods: A was conducted, synthesizing data from peer-reviewed literature expert commentary 2010 2024.Databases such PubMed, Cochrane Library, Google Scholar were searched for relevant studies.Results: spreads through airborne droplets contaminated surfaces, transmits direct contact infected bodily fluids.The response involves both innate adaptive systems, potentially leading a cytokine storm in severe cases.In contrast, evades system integrating into host cells, resulting infection progressive deterioration.Treatment focuses on symptom management prevention, antiviral medications vaccines playing crucial roles.Conversely, relies antiretroviral therapy (ART) suppress viral replication maintain function. Conclusion:The highlights nature versus progression HIV.Tailored prevention essential effective disease management.Recommendations: Public should address unique transmission routes viruses.Further research vaccine development therapeutic interventions is critical improving management.

Language: Английский

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CD4+ T cells facilitate replication of primary HIV-1 strains in macrophages and formation of macrophage internal virus-containing compartments

Journal of Virology, Journal Year: 2025, Volume and Issue: unknown

Published: March 25, 2025

ABSTRACT HIV-1 replication in macrophages is highly variable with internal virus accumulation so-called virus-containing compartments (VCCs). VCCs represent a reservoir that shielded from the antiviral immune response. VCC formation has been studied lab-adapted HIV-1, but it not investigated whether primary strains induce VCCs. Furthermore, although transmit to CD4+ T cells, effect of cells on unknown. We analyzed ability and replicate macrophages, non-infected cell coculture, formation. All replicated whereas only efficiently macrophage monocultures. Coculture enhanced process associated increased dependent direct cell-to-cell contact. Broadly neutralizing antibodies differentially affected cell-mediated enhancement macrophages. CD4 antibody treatment phenocopied infection-promoting coculture. In conclusion, facilitate induction appears be proxy for this phenotype. are promoted by CD4- GP120-dependent manner. Our findings highlight critical role cell-macrophage interaction dynamics call strategies interfere order target IMPORTANCE Here, we focus intimate interplay between HIV-1-infected cells. Specifically, (VCCs) within which thought serve as viral sanctuaries reservoirs. Notably, were unable unless they cocultured leading replication. This suggests an essential facilitating data importance addressing latent also targeting achieve ultimate goal functional cure.

Language: Английский

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The CLIC/GEEC pathway regulates particle uptake and formation of the virus-containing compartment (VCC) in HIV-1-infected macrophages

PLoS Pathogens, Journal Year: 2025, Volume and Issue: 21(3), P. e1012564 - e1012564

Published: March 11, 2025

HIV-1 particles are captured by the immunoglobulin superfamily member Siglec-1 on surface of macrophages and dendritic cells, leading to particle internalization facilitating trans-infection CD4+ T cells. HIV-1-infected develop a unique intracellular compartment termed virus-containing (VCC) that exhibits characteristic markers late endosome is enriched in components plasma membrane (PM). The VCC has been proposed as major site assembly macrophages. Depleting from significantly reduces formation, implying link between capture uptake external development VCCs within HIV-infected We found was independent clathrin, but required dynamin-2. CD98 CD44, classical CLIC/GEEC pathway, colocalized with VCC. Virus-like (VLPs) were taken up Siglec-1-enriched tubular membranes migrated centripetally over time form VCC-like structures. Inhibition CLIC/GEEC-mediated endocytosis resulted arrest macrophage cell surface, prevented reduced efficiency These findings indicate following virus Siglec-1, follow an endocytic route requires both pathway propose model which together leads formation macrophages, creating platform facilitates further budding.

Language: Английский

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Immuno-cell metabolic changes in HIV-1 infection

Infectious Diseases & Immunity, Journal Year: 2025, Volume and Issue: unknown

Published: March 12, 2025

Abstract Recent research has shown that metabolic processes within immune cells are essential for both human immunodeficiency virus 1 (HIV-1) infection and the response. Throughout HIV-1 infection—from acute stages to chronic viral latency—immune experience shifts in energy demands pathways, paralleling T-cell exhaustion. Dysregulated metabolism compromises cell function, leading dysfunction persistent inflammation. Therefore, alterations constitute a critical mechanism progression This review specifically explores profiles roles of T cells, monocytes-macrophages, dendritic natural killer B at different infection, emphasizing effects on pathways diverse types. These insights offer valuable therapeutic strategies aimed inhibiting replication, restoring controlling disease progression.

Language: Английский

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mRNA vaccines against HIV: Hopes and challenges

HIV Medicine, Journal Year: 2025, Volume and Issue: unknown

Published: April 7, 2025

Abstract Background Since the introduction of first licensed mRNA‐based vaccines against COVID‐19, there has been significant interest in leveraging this technology for other vaccines. An unprecedented surge mRNA emerged preclinical, clinical, and various research phases since 2020. The rapid development formulations, delivery methods, manufacturing processes made trend foreseeable. There is an urgent demand effective easily transportable regions where virus prevalent, shows promise addressing need. Methodology data was retrieved from databases, including Google Scholar, PubMed, Science Direct, ClinicalTrials.gov, government websites. following terms were used search strategies: HIV, vaccines, clinical trials, preclinical trials. A total 35 articles identified subsequently screened regarding HIV. Results are solution HIV treatment, as demonstrated by studies referenced article. Conclusion This review evaluates current state HIV‐1 vaccine development, clarifies targeting strategies, highlights recent findings, provides insights into challenges potential solutions associated with these issues. In review, we have explored focusing on their functional structure, design, manufacturing, distribution methodologies.

Language: Английский

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HIV-1 cell-to-cell infection of macrophages escapes type I interferon and host restriction factors, and is resistant to antiretroviral drugs

PLoS Pathogens, Journal Year: 2025, Volume and Issue: 21(4), P. e1013130 - e1013130

Published: April 28, 2025

HIV-1-infected macrophages participate in viral transmission, dissemination, and establishment of tissue virus reservoirs. Despite counteracting proteins (Vif, Vpu, Vpr Nef), cell-free macrophage infection is restricted by host cell factors, including those induced interferons. Here, we show that these type I interferon do not influence HIV-1 cell-to-cell transfer to cell-cell fusion with infected T cells, still leading the formation multinucleated giant cells (MGCs). Accordingly, depletion SERINC5 APOBEC3G alter spreading virus-producing MGCs. We further nuclei derived from remains transcriptionally active MGCs may explain resistance restriction factors antiretroviral drugs. Unexpectedly, detect DNA myeloid shortly after initial macrophages. Together, findings unravel how escapes cellular independently auxiliary proteins, while displaying

Language: Английский

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Additive Effects of Glutathione in Improving Antibiotic Efficacy in HIV–M.tb Co-Infection in the Central Nervous System: A Systematic Review

Viruses, Journal Year: 2025, Volume and Issue: 17(1), P. 127 - 127

Published: Jan. 17, 2025

Background: HIV and tuberculosis (TB) co-infection poses a significant health challenge, particularly when involving the central nervous system (CNS), where it leads to severe morbidity mortality. Current treatments face challenges such as drug resistance, immune reconstitution inflammatory syndrome (IRIS), persistent inflammation. Glutathione (GSH) has therapeutic potential enhance treatment outcomes by improving antibiotic efficacy, reducing inflammation, mitigating dysfunction. Methods: Relevant studies were identified through systematic searches of PubMed, Elsevier, WHO, related databases. Inclusion criteria focused on preclinical clinical research examining GSH or its precursors in HIV, TB, co-infection, with emphasis microbial control, modulation, CNS-related outcomes. Results: Preclinical showed that improves macrophage antimicrobial function, reduces oxidative stress, limits Mycobacterium (M.tb) growth. Animal models demonstrated reduced bacterial burden lungs, liver, spleen supplementation, along enhanced granuloma stability. Clinical highlighted increased TH1 cytokine production, markers, improved CD4+ T cell counts HIV–M.tb co-infected patients. N-acetylcysteine (NAC), precursor, was shown significantly efficacy first-line TB antibiotics mitigate treatment-associated toxicity. Discussion: shows promise an adjunct therapy for cases CNS, may improve recovery reduce However, evidence is limited small sample sizes lack randomized trials. Future should focus developing CNS-directed formulations evaluating integration into current protocols address dual ultimately patient

Language: Английский

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Activated THP-1 Macrophage-Derived Factors Increase the Cytokine, Fractalkine, and EGF Secretions, the Invasion-Related MMP Production, and Antioxidant Activity of HEC-1A Endometrium Cells

International Journal of Molecular Sciences, Journal Year: 2024, Volume and Issue: 25(17), P. 9624 - 9624

Published: Sept. 5, 2024

Endometrium receptivity is a multifactor-regulated process involving progesterone receptor-regulated signaling, cytokines and chemokines, additional growth regulatory factors. In the female reproductive system, macrophages have distinct roles in regulation of receptivity, embryo implantation, immune tolerance, angiogenesis or oxidative stress. present study, we investigated effects PMA-activated THP-1 on receptivity-related genes, regulators, stress-related molecules HEC-1A endometrium cells. We established non-contact co-culture which culture medium exhibiting pro-inflammatory phenotype was used for treatment endometrial cells, expression growth-related factors activin bone morphogenetic protein 2, hormone EGF, activation downstream signaling pERK1/2 pAkt were analyzed by ELISA Western blot. The secretions are involved establishment matrix metalloproteinases implicated invasion also determined. Based results, may play role They alter secretion as well level MMPs Moreover, activated elevate stress protection All these suggest that special implantation-related

Language: Английский

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The CLIC/GEEC pathway regulates particle endocytosis and formation of the virus-containing compartment (VCC) in HIV-1-infected macrophages

bioRxiv (Cold Spring Harbor Laboratory), Journal Year: 2024, Volume and Issue: unknown

Published: Sept. 5, 2024

Abstract HIV-1 particles are captured by the immunoglobulin superfamily member Siglec-1 on surface of macrophages and dendritic cells, leading to particle internalization facilitating trans-infection CD4+ T cells. HIV-1-infected develop a unique intracellular compartment termed virus-containing (VCC) that exhibits characteristic markers late endosome is enriched in components plasma membrane (PM). The VCC has been proposed as major site assembly macrophages. Depleting from significantly reduces formation, implying link between capture endocytosis external development VCCs within HIV-infected We found was independent clathrin, but required dynamin-2. CD98 CD44, classical CLIC/GEEC pathway, colocalized with VCC. Inhibition CLIC/GEEC-mediated chemical or genetic means resulted arrest macrophage cell prevented formation. Virus-like (VLPs) were taken up Siglec-1-enriched tubular membranes migrated centripetally over time form VCC-like structures. These findings indicate following virus Siglec-1, follow an endocytic route requires both pathway propose model which together leads formation macrophages, creating platform facilitates further budding. Author Summary types infected HIV cells Infection great interest because this type can contribute transmission tissues, HIV-related complications include neurologic disorders, endocrine cardiovascular disease. infection may also create latent reservoir persists individuals despite administration antiretroviral therapy. Here we focused forms described holding for viruses, contains organelles membrane. identified helps explain origins VCC, pathway. virus-like delivery forming GTPase dynamin-2 This study identifies new facet how interacts suggesting disruption could be therapeutic strategy implications cure efforts.

Language: Английский

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Pro-inflammatory macrophages suppress HIV replication in humanized mice and ex vivo co-cultures

Frontiers in Immunology, Journal Year: 2024, Volume and Issue: 15

Published: Nov. 7, 2024

Introduction Very little is known about the role of macrophages as immune mediators during natural HIV infection. Humanized mice are an extremely valuable in vivo model for studying pathogenesis. However, presence murine mononuclear phagocytes these models represents a significant limitation their human counterpart. Therefore, we have developed novel humanized mouse that allows selective depletion myeloid cells at time point our choosing. Methods We genetically engineered hematopoietic stem and progenitor (HSPCs) to express inducible caspase-9 (iCas9) suicide system under synthetic promoter. Using HSPCs, generated mice. iCasp9 induction resulted cell death this (iHMD) model. In addition, co-cultured monocyte-derived with ex HIV-infected PBMCs further mechanistically investigate effect on replication using flow cytometry, cytokine analysis, RNA sequencing both CD4+ T cells. Results infection induced pro-inflammatory phenotype NSG early late stages Myeloid iHMD-NSG rapid increase replication, which was accompanied by loss cytokines. Co-culture reproduced anti-HIV effects observed . Transcriptomic data showed upregulate antiviral cytokines chemokines co-culture, while inducing restriction factors downregulate pathways involved protein expression replication. Discussion This study describes effector cells, , acting against limiting disease progression.

Language: Английский

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