A possible overwintering mechanism for bluetongue virus in the absence of the insect vector

• Published in: Journal of general virology Vol. 84; no. 1; pp. 227 - 235
• Main Authors: Takamatsu, H, Mellor, P. S, Mertens, P. P. C, Kirkham, P. A, Burroughs, J. N, Parkhouse, R. M. E
• Format: Journal Article
• Language: English
• Published: England Soc General Microbiol 01-01-2003
• Subjects: Animals; Bluetongue - transmission; Bluetongue - virology; Bluetongue virus; Bluetongue virus - physiology; Cattle; Cell Line; Ceratopogonidae - physiology; Ceratopogonidae - virology; Coculture Techniques; Culicoides; Fibroblasts - virology; Freshwater; Insect Vectors - physiology; Insect Vectors - virology; Orbivirus; Receptors, Antigen, T-Cell, gamma-delta - metabolism; Seasons; Sheep; Skin - cytology; Skin - virology; T-Lymphocytes - virology
• ISSN: 0022-1317; 1465-2099
• DOI: 10.1099/vir.0.18705-0

Institute for Animal Health, Pirbright Laboratory, Woking, Surrey GU24 0NF, UK
Correspondence Peter Mertens peter.mertens{at}bbsrc.ac.uk
Bluetongue virus (BTV) and several other Orbivirus species are transmitted between mammalian hosts via bites from adults of certain species of Culicoides midges. However, BTV can survive for 9–12 months (typically during the winter), in the absence of adult vectors, with no detectable cases of viraemia, disease or seroconversion in the host. The survival of the virus from one ‘vector season’ to the next is called ‘overwintering’ but the mechanism involved is not fully understood. It is demonstrated that BTV can persistently infect ovine T-cells in vitro , a process that may also occur during infection and viraemia in mammalian hosts, thus providing a mechanism for virus persistence. Interaction of persistently BTV-infected T-cells with antibody to the T-cell-specific surface molecule WC-1 resulted in conversion to a lytic infection and increased virus release. Skin fibroblasts induce a similar conversion, indicating that they express a counter ligand for WC-1. Feeding of Culicoides midges induces skin inflammation, which is accompanied by recruitment of large numbers of activated T-cells. The interaction of persistently infected T-cells with skin fibroblasts would result in increased virus production at ‘biting sites’, favouring transmission to the insect vector. This suggested mechanism might also involve up-regulation of the WC-1 ligand at inflamed sites. It has been shown previously that cleavage of virus surface proteins by protease enzymes (which may also be associated with inflammation) generates infectious subvirus particles that have enhanced infectivity (100 times) for the insect vector.
Present address : Novartis Horsham Research Centre, Wimblehurst Road, Horsham, West Sussex RH12 4AB, UK.
Present address : Instituto Gulbenkian de Ciencia, Aportado 14, 2781 Oeiras Codex, Portugal.
Published ahead of print on 15 October 2002 as DOI 10.1099/vir.0.18705-0.