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10.3390/v14050996

http://scihub22266oqcxt.onion/10.3390/v14050996
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35632738!9143815!35632738
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suck abstract from ncbi


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pmid35632738      Viruses 2022 ; 14 (5): ä
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  • High Expression of HERV-K (HML-2) Might Stimulate Interferon in COVID-19 Patients #MMPMID35632738
  • Guo Y; Yang C; Liu Y; Li T; Li H; Han J; Jia L; Wang X; Zhang B; Li J; Li L
  • Viruses 2022[May]; 14 (5): ä PMID35632738show ga
  • Background. Interferon is a marker of host antiviral immunity, which is disordered in COVID-19 patients. ERV can affect the secretion of interferon through the cGAS-STING pathway. In this study, we explored whether IFN-I and HERV-K (HML-2) were activated in COVID-19 patients and whether there was an interaction between them. Methods. We collected blood samples from COVID-19 patients and healthy controls. We first detected the expression of HERV-K (HML-2) gag, env, and pol genes and IFN-I-related genes between patients and healthy people by qPCR, synchronously detected VERO cells infected with SARS-CoV-2. Then, the chromosome distributions of highly expressed HERV-K (HML-2) gag, env, and pol genes were mapped by the next-generation sequencing results, and GO analysis was performed on the related genes. Results. We found that the HERV-K (HML-2) gag, env, and pol genes were highly expressed in COVID-19 patients and VERO cells infected with SARS-CoV-2. The interferon-related genes IFNB1, ISG15, and IFIT1 were also activated in COVID-19 patients, and GO analysis showed that HERV-K (HML-2) can regulate the secretion of interferon. Conclusions. The high expression of HERV-K (HML-2) might activate the increase of interferon in COVID-19 patients, proving that HERV-K does not only play a negative role in the human body.
  • |*COVID-19/virology[MESH]
  • |*Endogenous Retroviruses/genetics[MESH]
  • |*Interferons/genetics[MESH]
  • |Animals[MESH]
  • |Antiviral Agents[MESH]
  • |Chlorocebus aethiops[MESH]
  • |Genes, Viral[MESH]
  • |Humans[MESH]
  • |SARS-CoV-2[MESH]


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