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Autophagy induction regulates influenza virus replication in a time-dependent manner

Feizi, Neda (författare)
Pasteur Institute of Iran
Mehrbod, Parvaneh (författare)
Pasteur Institute of Iran
Romani, Bizhan (författare)
University of Alberta,Ahvaz, Jundishapur University of Medical Sciences
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Soleimanjahi, Hoorieh (författare)
Tarbiat Modares University
Bamdad, Taravat (författare)
Tarbiat Modares University
Feizi, Amir, 1980 (författare)
Chalmers tekniska högskola,Chalmers University of Technology
Jazaeri, Ehsan Ollah (författare)
Pasteur Institute of Iran
Targhi, Hadiseh Shokouhi (författare)
Pasteur Institute of Iran
Saleh, Maryam (författare)
Pasteur Institute of Iran
Jamali, Abbas (författare)
Pasteur Institute of Iran
Fotouhi, Fatemeh (författare)
Pasteur Institute of Iran
Nargesabad, Reza Nasrollahi (författare)
Pasteur Institute of Iran
Abdoli, Asghar (författare)
Pasteur Institute of Iran
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 (creator_code:org_t)
Microbiology Society, 2017
2017
Engelska.
Ingår i: Journal of Medical Microbiology. - : Microbiology Society. - 0022-2615 .- 1473-5644. ; 66:4, s. 536-541
  • Tidskriftsartikel (refereegranskat)
Abstract Ämnesord
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  • Purpose. Autophagy plays a key role in host defence responses against microbial infections by promoting degradation of pathogens and participating in acquired immunity. The interaction between autophagy and viruses is complex, and this pathway is hijacked by several viruses. Influenza virus (IV) interferes with autophagy through its replication and increases the accumulation of autophagosomes by blocking lysosome fusion. Thus, autophagy could be an effective area for antiviral research. Methodology. In this study, we evaluated the effect of autophagy on IV replication. Two cell lines were transfected with Beclin-1 expression plasmid before (prophylactic approach) and after (therapeutic approach) IV inoculation. Results/Key findings. Beclin-1 overexpression in the cells infected by virus induced autophagy to 26 %. The log10 haemagglutinin titre and TCID50 (tissue culture infective dose giving 50% infection) of replicating virus were measured at 24 and 48 h post-infection. In the prophylactic approach, the virus titre was enhanced significantly at 24 h post-infection (P?0.01), but it was not significantly different from the control at 48 h post-infection. In contrast, the therapeutic approach of autophagy induction inhibited the virus replication at 24 and 48 h post-infection. Additionally, we showed that inhibition of autophagy using 3-methyladenine reduced viral replication. Conclusion. This study revealed that the virus (H1N1) titre was controlled in a time-dependent manner following autophagy induction in host cells. Manipulation of autophagy during the IV life cycle can be targeted both for antiviral aims and for increasing viral yield for virus production.

Ämnesord

NATURVETENSKAP  -- Biologi -- Immunologi (hsv//swe)
NATURAL SCIENCES  -- Biological Sciences -- Immunology (hsv//eng)
MEDICIN OCH HÄLSOVETENSKAP  -- Klinisk medicin -- Infektionsmedicin (hsv//swe)
MEDICAL AND HEALTH SCIENCES  -- Clinical Medicine -- Infectious Medicine (hsv//eng)
MEDICIN OCH HÄLSOVETENSKAP  -- Medicinska och farmaceutiska grundvetenskaper -- Mikrobiologi inom det medicinska området (hsv//swe)
MEDICAL AND HEALTH SCIENCES  -- Basic Medicine -- Microbiology in the medical area (hsv//eng)

Nyckelord

Autophagy
Replication
Influenza virus
Beclin-1

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