Show simple item record

dc.contributor.authorMartins, Laura J
dc.contributor.authorSzaniawski, Matthew A
dc.contributor.authorWilliams, Elizabeth S C P
dc.contributor.authorCoiras, Mayte 
dc.contributor.authorHanley, Timothy M
dc.contributor.authorPlanelles, Vicente
dc.identifier.citationPathogens. 2022 Jan 26;11(2):163.es_ES
dc.description.abstractHIV-1 infection of myeloid cells is associated with the induction of an IFN response. How HIV-1 manipulates and subverts the IFN response is of key interest for the design of therapeutics to improve immune function and mitigate immune dysregulation in people living with HIV. HIV-1 accessory genes function to improve viral fitness by altering host pathways in ways that enable transmission to occur without interference from the immune response. We previously described changes in transcriptomes from HIV-1 infected and from IFN-stimulated macrophages and noted that transcription of IFN-regulated genes and genes related to cell cycle processes were upregulated during HIV-1 infection. In the present study, we sought to define the roles of individual viral accessory genes in upregulation of IFN-regulated and cell cycle-related genes using RNA sequencing. We observed that Vif induces a set of genes involved in mitotic processes and that these genes are potently downregulated upon stimulation with type-I and -II IFNs. Vpr also upregulated cell cycle-related genes and was largely responsible for inducing an attenuated IFN response. We note that the induced IFN response most closely resembled a type-III IFN response. Vpu and Nef-regulated smaller sets of genes whose transcriptomic signatures upon infection related to cytokine and chemokine processes. This work provides more insight regarding processes that are manipulated by HIV-1 accessory proteins at the transcriptional level.es_ES
dc.description.sponsorshipThis research was partially funded by the National Institutes of Health, grants AI143567-02 (V.P. and M.C.) and AI122377-05 (V.P.) and by startup funds from the Department of Pathology, University of Utah School of Medicine (T.M.H.).es_ES
dc.publisherMultidisciplinary Digital Publishing Institute (MDPI) es_ES
dc.subjectAccessory proteinses_ES
dc.subjectCell cyclees_ES
dc.subjectInnate immunees_ES
dc.titleHIV-1 Accessory Proteins Impart a Modest Interferon Response and Upregulate Cell Cycle-Related Genes in Macrophageses_ES
dc.typejournal articlees_ES
dc.rights.licenseAtribución 4.0 Internacional*
dc.contributor.funderNational Institutes of Health (Estados Unidos) es_ES
dc.contributor.funderUniversity of Utah (Estados Unidos) es_ES
dc.identifier.journalPathogens (Basel, Switzerland)es_ES
dc.repisalud.centroISCIII::Centro Nacional de Microbiologíaes_ES
dc.rights.accessRightsopen accesses_ES

Files in this item

Acceso Abierto

This item appears in the following Collection(s)

Show simple item record

Atribución 4.0 Internacional
This item is licensed under a: Atribución 4.0 Internacional