ArticleRetrovirology2007
Differential resistance to cell entry by porcine endogenous retrovirus subgroup A in rodent species.
Article in Retrovirology, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
What it found
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The trial behind it
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Who cites it
11 citing papers in PubMed, 26 citations in OpenAlex.
- Co-Cultivation Assays for Detecting Infectious Human-Tropic Porcine Endogenous Retroviruses (PERVs).International journal of molecular sciences · 2025Review
- Riboflavin transporter: evidence of a role as entry receptor for chimpanzee endogenous retrovirus.Virus evolution · 2025Article
- Rare isolation of human-tropic recombinant porcine endogenous retroviruses PERV-A/C from Göttingen minipigs.Virology journal · 2022Article
- Review
- Why was PERV not transmitted during preclinical and clinical xenotransplantation trials and after inoculation of animals?Retrovirology · 2018Review
- Role of DNA methylation in expression and transmission of porcine endogenous retroviruses.Journal of virology · 2013Article
- Article
- Microbiological safety of a novel bio-artificial liver support system based on porcine hepatocytes: a experimental study.European journal of medical research · 2012Article
- Infection barriers to successful xenotransplantation focusing on porcine endogenous retroviruses.Clinical microbiology reviews · 2012Review
- Suboptimal porcine endogenous retrovirus infection in non-human primate cells: implication for preclinical xenotransplantation.PloS one · 2010Article
- Identification of two distinct structural regions in a human porcine endogenous retrovirus receptor, HuPAR2, contributing to function for viral entry.Retrovirology · 2009Article
Corrections and comments
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Authors and funding
3 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundThe risk of zoonotic infection by porcine endogenous retroviruses (PERV) has been highlighted in the context of pig-to-human xenotransplantation. The use of receptors for cell entry often determines the host range of retroviruses. A human-tropic PERV subgroup, PERV-A, can enter human cells through either of two homologous multitransmembrane proteins, huPAR-1 and huPAR-2. Here, we characterised human PARs and their homologues in the PERV-A resistant rodent species, mouse and rat (muPAR and ratPAR, respectively).
resultsUpon exogenous expression in PERV-A resistant cells, human and rat PARs, but not muPAR, conferred PERV-A sensitivity. Exogenously expressed ratPAR binds PERV-A Env and allows PERV-A infection with equivalent efficiency to that of huPAR-1. Endogenous ratPAR expression in rat cell lines appeared to be too low for PERV-A infection. In contrast, the presence of Pro at position 109 in muPAR was identified to be the determinant for PERV-A resistance. Pro109. was shown to be located in the second extracellular loop (ECL2) and affected PERV-A Env binding to PAR molecules.
conclusionThe basis of resistance to PERV-A infection in two rodent species is different. Identification of a single a.a. mutation in muPAR, which is responsible for mouse cell resistance to PERV-A highlighted the importance of ECL-2 for the viral receptor function.
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