The reservoir host of cowpox virus in Western Europe is not known, but epidemiological evidence from human and feline infections indicates that the virus is probably endemic in small wild rodents. Therefore, serum and tissue samples were collected from a variety of wild British mammals and some birds, and tested for evidence of Orthopoxvirus infection. Antibody reacting with cowpox virus was detected in 9/44 (20%) bank voles (Clethrionomys glareolus), 8/24 (33%) field voles (Microtus agrestis), 17/86 (20%) wood mice (Apodemus sylvaticus) and 1/44 house mice (Mus musculus), but in no other animal species tested. Although virus was not isolated from any animal, this serological survey, together with other evidence, suggests that bank and field voles and wood mice are the main reservoir hosts of cowpox virus in Great Britain.

No abstract

Feline calicivirus (FCV) is a highly infectious respiratory pathogen of domestic cats. The prevalence of FCV in the general cat population is high, particularly in multi-cat households, largely because many clinically recovered cats remain persistently infected carriers. In order to assess how FCV circulates in such groups and to assess the contribution that each individual animal makes to the epidemiology of the disease, we have carried out the first detailed analysis of long-term shedding patterns of FCV in individual cats within naturally infected colonies. The prevalence of FCV in each of the groups on individual sampling occasions ranged from 0% to 91%, with averages for the individual colonies ranging from 6% to 75%. Within each of the colonies, one to three distinct strains of FCV were identified. Individual cats showed a spectrum of FCV shedding patterns over the sampling period which broadly grouped into three categories: those that shed virus relatively consistently, those that shed virus intermittently, and those that appeared never to shed virus. This is the first report identifying non-shedder cats that appear resistant to FCV infection over long periods of time, despite being continually exposed to virus. Such resistance appeared to be age related, which may have been immune-mediated, although by analogy with other caliciviruses, factors such as host genetic resistance may play a role. Given that a proportion of the population appears to be resistant to infection, clearly the cohort of cats that consistently shed virus are likely to provide an important mechanism whereby infection can be maintained in small populations.

Infection of laboratory mice by the Murid herpesvirus 4 (MHV-4) is a much studied model system for gammaherpesvirus pathogenesis. Little, however, is known about its natural host range, epidemiology and pathogenesis outside the laboratory. We have studied MHV-4 infection in freeliving murids in the UK. Using a combination of serology and PCR analysis, we found that MHV-4 was endemic in wood mice (Apodemus sylvaticus) but not in two species of voles (Clethrionomys glareolus, Microtus agrestis). The sites of detection of viral DNA were the lungs and, less commonly, the spleen, emphasizing the importance of the former in virus persistence during natural infection and confirming similar data in laboratory mice.

In order to map linear B-cell (LBC) epitopes in the major capsid protein of feline calicivirus (FCV), an expression library containing random, short (100- to 200-bp) fragments of the FCV F9 capsid gene was constructed. Analysis of this library showed it to be representative of the region of the capsid gene that encodes the mature capsid protein. The library was screened by using polyclonal antisera from a cat that had been challenged experimentally with F9 to identify immunoreactive clones containing LBC epitopes. Twenty-six clones that reacted positively to feline antisera in immunoblots were identified. FCV-derived sequence from these clones mapped to a region of the capsid that spanned 126 amino acids and included variable regions C and E. An overlapping set of biotinylated peptides corresponding to this region was used to further map LBC epitopes by using F9 antisera. Four principal regions of reactivity were identified. Two fell within the hypervariable region at the 5′ end of region E (amino acids [aa] 445 to 451 [antigenic site {ags} 2] and aa 451 to 457 [ags 3]). However, the other two were in conserved regions (aa 415 to 421 [ags 1; region D] and aa 475 to 479 [ags 4; central region E]). The reactivity of the peptide set with antisera from 11 other cats infected with a range of FCV isolates was also determined. Ten of 11 antisera reacted to conserved ags 4, suggesting that this region may be useful for future recombinant vaccine design.