دورية أكاديمية
أعرض في EDS

Adaptation of SIVmac to baboon primary cells results in complete absence of in vivo baboon infectivity.

التفاصيل البيبلوغرافية
العنوان: Adaptation of SIVmac to baboon primary cells results in complete absence of in vivo baboon infectivity.
المؤلفون: Obregon-Perko V; Texas Biomedical Research Institute, San Antonio, TX, United States., Mannino A; Texas Biomedical Research Institute, San Antonio, TX, United States., Ladner JT; The Pathogen and Microbiome Institute, Northern Arizona University, Flagstaff, AZ, United States., Hodara V; Texas Biomedical Research Institute, San Antonio, TX, United States., Ebrahimi D; Texas Biomedical Research Institute, San Antonio, TX, United States., Parodi L; Texas Biomedical Research Institute, San Antonio, TX, United States., Callery J; Department of Biology, Trinity University, San Antonio, TX, United States., Palacios G; Icahn School of Medicine at Mount Sinai, New York, NY, United States., Giavedoni LD; Department of Biology, Trinity University, San Antonio, TX, United States.
المصدر: Frontiers in cellular and infection microbiology [Front Cell Infect Microbiol] 2024 Jun 28; Vol. 14, pp. 1408245. Date of Electronic Publication: 2024 Jun 28 (Print Publication: 2024).
نوع المنشور: Journal Article
اللغة: English
بيانات الدورية: Publisher: Frontiers Media SA Country of Publication: Switzerland NLM ID: 101585359 Publication Model: eCollection Cited Medium: Internet ISSN: 2235-2988 (Electronic) Linking ISSN: 22352988 NLM ISO Abbreviation: Front Cell Infect Microbiol Subsets: MEDLINE
أسماء مطبوعة: Original Publication: Lausanne : Frontiers Media SA
مواضيع طبية MeSH: Simian Immunodeficiency Virus*/genetics , Simian Immunodeficiency Virus*/physiology , Virus Replication* , Simian Acquired Immunodeficiency Syndrome*/virology , Simian Acquired Immunodeficiency Syndrome*/immunology , Papio*, Animals ; Leukocytes, Mononuclear/virology ; Leukocytes, Mononuclear/immunology ; Receptors, CCR5/metabolism ; Receptors, CCR5/genetics ; CD4-Positive T-Lymphocytes/virology ; CD4-Positive T-Lymphocytes/immunology ; Cells, Cultured ; Serial Passage
مستخلص: While simian immunodeficiency virus (SIV) infection is non-pathogenic in naturally infected African nonhuman primate hosts, experimental or accidental infection in rhesus macaques often leads to AIDS. Baboons, widely distributed throughout Africa, do not naturally harbor SIV, and experimental infection of baboons with SIVmac results in transient low-level viral replication. Elucidation of mechanisms of natural immunity in baboons could uncover new targets of antiviral intervention. We tested the hypothesis that an SIVmac adapted to replicate in baboon primary cells will gain the capacity to establish chronic infections in vivo . Here, we generated SIVmac variants in baboon cells through serial passage in PBMC from different donors (SIVbn-PBMC s1), in PBMC from the same donors (SIVbn-PBMC s2), or in isolated CD4 cells from the same donors used for series 2 (SIVbn-CD4). While SIVbn-PBMC s1 and SIVbn-CD4 demonstrated increased replication capacity, SIVbn-PBMC s2 did not. Pharmacological blockade of CCR5 revealed SIVbn-PBMC s1 could more efficiently use available CCR5 than SIVmac, a trait we hypothesize arose to circumvent receptor occupation by chemokines. Sequencing analysis showed that all three viruses accumulated different types of mutations, and that more non-synonymous mutations became fixed in SIVbn-PBMC s1 than SIVbn-PBMC s2 and SIVbn-CD4, supporting the notion of stronger fitness pressure in PBMC from different genetic backgrounds. Testing the individual contribution of several newly fixed SIV mutations suggested that is the additive effect of these mutations in SIVbn-PBMC s1 that contributed to its enhanced fitness, as recombinant single mutant viruses showed no difference in replication capacity over the parental SIVmac239 strain. The replicative capacity of SIVbn-PBMC passage 4 (P4) s1 was tested in vivo by infecting baboons intravenously with SIVbn-PBMC P4 s1 or SIVmac251. While animals infected with SIVmac251 showed the known pattern of transient low-level viremia, animals infected with SIVbn-PBMC P4 s1 had undetectable viremia or viral DNA in lymphoid tissue. These studies suggest that adaptation of SIV to grow in baboon primary cells results in mutations that confer increased replicative capacity in the artificial environment of cell culture but make the virus unable to avoid the restrictive factors generated by a complex multicellular organism.
Competing Interests: The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.
(Copyright © 2024 Obregon-Perko, Mannino, Ladner, Hodara, Ebrahimi, Parodi, Callery, Palacios and Giavedoni.)
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فهرسة مساهمة: Keywords: baboon; chronic infection; innate immunity; simian immunodeficiency virus (SIV); viral adaptive changes and evolution
المشرفين على المادة: 0 (Receptors, CCR5)
تواريخ الأحداث: Date Created: 20240715 Date Completed: 20240715 Latest Revision: 20240716
رمز التحديث: 20240716
مُعرف محوري في PubMed: PMC11239360
DOI: 10.3389/fcimb.2024.1408245
PMID: 39006742
قاعدة البيانات: MEDLINE
الوصف
تدمد:2235-2988
DOI:10.3389/fcimb.2024.1408245