| dc.description.abstract | Autophagy is an evolutionary conserved process for the recycling of cellular contents through the delivery of the targeted structures to the lysosome for degradation. Research on autophagy started in the late 1950s but only within the last two decades, the interaction between viruses and autophagy has become a topic of interest. Autophagy was shown to play a key role during the immune response against group A Streptococcus bacteria and the parasite Toxoplasma by preventing their replication. Additionally sinbis virus infection is compromised by autophagy. Conversely, autophagy was also proven to be pro-viral stimulating viral yields of both polio and dengue virus, amongst others. These observations have indicated that specific viruses can manipulate autophagy either positively or negatively in order to enhance their own replication. In this thesis the interaction between autophagy and four different viruses, i.e. herpes, vaccinia corona and influenza virus has been discussed. Herpesviruses can be divided into three categories: alpha, beta and gamma, and each class of herpesvirus display some similar characteristics regarding the interplay with autophagy. Differences are, however, also present. These differences cannot only be found between classes, but also within classes as well as between infections in different cell types. Interaction of vaccinia viruses and coronaviruses are less well defined compared to those of the herpesviruses. Although evidence exists for autophagy manipulation by vaccinia viruses, this has not been clarified for coronaviruses. Nonetheless within the coronavirus life cycle an autophagy protein but not an intact autophagy machinery, was shown to be involved in the replication of the virus suggesting that autophagy proteins may be involved in other cellular processes as well. Studies on the influenza virus have generated some conflicting data where a block in autophagy was shown by some research groups while others revealed the contrary. Discrepancies are, nevertheless, not only present in literature about the influenza virus but are also seen in that of herpesviruses. This could be due to the virus behaving differently when infecting different cell types. Current knowledge on the interaction between autophagy and these different viruses will be reviewed in this thesis along with the discussion of the discrepancies and models suggesting possible future lines of research. | |
