Human papillomavirus infection is inhibited by host autophagy in primary human keratinocytes
| Autor: | Dohun Pyeon, Laura M. Griffin, Louis Cicchini |
|---|---|
| Rok vydání: | 2013 |
| Předmět: |
HFK
Keratinocytes HPV Autophagosome viruses Entry Ubiquitin-Activating Enzymes Biology Autophagy-Related Protein 7 Article Virus Cell Line Phosphatidylinositol 3-Kinases Virology Autophagy medicine Humans RNA Small Interfering 3-MA Cells Cultured Infectivity Human papillomavirus 16 Gene knockdown Trafficking integumentary system Adenine 3-methyladenine virus diseases Papillomavirus Virus Internalization female genital diseases and pregnancy complications Cell biology HaCaT HEK293 Cells medicine.anatomical_structure Cell culture Capsid Proteins RNA Interference Keratinocyte |
| Zdroj: | Virology. 437:12-19 |
| ISSN: | 0042-6822 |
| DOI: | 10.1016/j.virol.2012.12.004 |
| Popis: | Human papillomavirus (HPV) infection is severely limited in its natural host, primary human keratinocytes. Our data show HPV infectivity in primary keratinocytes is over 100- and 1,000-fold lower than in established keratinocyte cell lines NIKS and HaCaT, respectively. Here, we show that the basal level of autophagy in primary human foreskin keratinocytes (HFKs) is higher than in immortalized keratinocytes, and that HPV16 virions significantly induce autophagy in HFKs. Interestingly, HPV16 infectivity is dramatically enhanced by knockdown of essential autophagy genes as well as biochemical inhibition of autophagy. The increase in HPV16 infectivity by autophagy inhibition is most significant in HFKs, showing an inverse correlation with basal HPV16 infectivity in HFK, NIKS, HaCaT, and 293FT cells. Further, inhibition of autophagy delays degradation of HPV16 capsid proteins during virus trafficking, indicating that host autophagy induced by HPV16 virions inhibits infection of primary keratinocytes through rapid degradation of viral capsid proteins. |
| Databáze: | OpenAIRE |
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