title: Are nidoviruses hijacking the autophagy machinery?
abstract: Autophagy is an intracellular catabolic transport route conserved among all eukaryotic cells. It has multiple important physiological functions, one of which is to act as an immune mechanism against intracellular microbes.(1,2) Bacteria and viruses targeted for destruction are sequestered into large double-membrane vesicles called autophagosomes and subsequently delivered to the lysosomes where they are consumed by resident hydrolases. Unfortunately, conserved cellular pathways are often exploited by pathogens to facilitate their entry or replication, and autophagy is no exception. It has become clear that certain bacteria and viruses subvert this process to their advantage.(3) Nidoviruses, which comprise coronaviruses and arteriviruses, might be among the successful. Long recognized as the cause of veterinary infections, this group of enveloped, positive-stranded RNA viruses is currently of considerable interest due to the emergence of new human coronaviruses, especially the severe acute respiratory syndrome (SARS)-coronavirus. In this mini-review, we will summarize the so far limited number of studies that have demonstrated that double-membrane vesicles resembling autophagosomes are the sites of nidovirus replication. In addition, we will discuss how the formation of these large vesicles might be induced.
authors.affiliation: Virology Division, Department of Infectious Diseases & Immunology, Faculty of Veterinary Medicine and Institute of Biomembranes, Utrecht University, Utrecht, The Netherlands.
authors.forename: Cornelis A M
authors.initials: CA
authors.lastname: de Haan
authors.forename: Fulvio
authors.initials: F
authors.lastname: Reggiori
mesh_terms: D000818:Animals; D001343:Autophagy / Q000502:physiology*; D004721:Endoplasmic Reticulum / Q000502:physiology / Q000648:ultrastructure; D006801:Humans; D028381:Nidovirales / Q000502:physiology*; D010588:Phagosomes / Q000502:physiology; D012327:RNA Virus Infections / Q000378:metabolism / Q000473:pathology / Q000821:virology; D014779:Virus Replication / Q000502:physiology