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Short Communication |

Division of Immunology and Genetics, The John Curtin School of Medical Research, Australian National University, Canberra, ACT 0200, Australia
Correspondence
Mohammed Alsharifi
mohammed.alsharifi{at}imvs.sa.gov.au
or
mohammed.alsharifi{at}anu.edu.au
Previously, we have shown that mice defective in granule exocytosis and/or Fas.L/Fas-mediated cytolytic pathways are significantly more resistant to alphavirus, Semliki Forest virus (SFV), infection compared with wild-type mice. Here, we evaluated SFV replication in different tissues of mice defective in both cytolytic pathways (perf–/–xgld) relative to that in wild-type counterparts and found that viral replication in perf–/–xgld mice is remarkably restricted. Although the mechanism responsible for this observation is yet to be established, the lower virus titres found in these mice indicate that the role of cytolytic effector molecules in antiviral immunity needs to be re-evaluated.
Present address: Infectious Diseases Laboratories, Institute of Medical and Veterinary Science, Royal Adelaide Hospital, Adelaide, SA 5000, Australia
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