J Virol. 2011 Mar 9. [Epub ahead of print]
Investigation of koi herpesvirus (KHV) latency in koi.
Eide KE, Miller-Morgan T, Heidel JR, Kent ML, Bildfell RJ, Lapatra S, Watson G, Jin L.
Department of Biomedical Sciences, College of Veterinary Medicine, Oregon State University, Corvallis, OR 97331; Department of Microbiology, College of Science, Oregon State University, Corvallis, OR 97331; Oregon Sea Grant Extension, Oregon State University, Corvallis, OR 97331; Research Division, Clear Springs Foods, Inc, Buhl, ID 83316.
Abstract
Koi Herpes Virus (KHV) has recently been classified as a member of the family of Alloherpesviridae within the order of Herpesvirales. One of the unique features of Herpesviridae is latent infection following a primary infection. However, KHV latency has not been recognized. To determine if latency occurs in clinically normal fish from facilities with a history of KHV infection or exposure, the presence of the KHV genome was investigated in healthy koi by PCR and Southern blot. KHV DNA, but not infectious virus or mRNAs from lytic infection, was detected in white blood cells from investigated koi. Virus shedding was examined via tissue culture and RT-PCR testing of gill mucus and feces from six koi every other day for one month. No infectious virus or KHV DNA was detected in fecal secretion or gill swabs, suggesting neither acute nor persistent infection was present. To determine if KHV latent infections can be reactivated, six koi were subjected to a temperature stress regime. KHV DNA and infectious virus were detected in both gill and fecal swabs by day 8 post-temperature stress. KHV DNA was also detectable in brain, spleen, gills, heart, eye, intestine, kidney, liver, and pancreas in euthanized koi one month post temperature stress. Our study suggests KHV may become latent in leukocytes and other tissues, can be reactivated from latency by temperature stress, and may be more widespread in the koi population than previously suspected.
PMID: 21389134 [PubMed - as supplied by publisher]