However, such measures generally do not entirely eliminate infection. Infection of neonatal goats with caprine arthritis encephalitis virus occurs through the ingestion of infective milk or colostrum, consequently the rate of infection of newborn goats can be dramatically reduced by removing goats from infected does at birth, providing pasteurized caprine colostrum/milk, or substituting cow’s milk. However, not all infected goats will develop clinically significant disease in their lifespan. Although both humoral and cellular immune responses can be effective in controlling the infection, the ability of the virus to persist through both antigenic variation and latency leads to lifelong persistent infection. In Fenner's Veterinary Virology (Fifth Edition), 2017 Immunity, Prevention, and ControlĬlearance of caprine arthritis encephalitis virus infection by host immune responses (eg, sterilizing immunity) does not generally occur because of stable integration of provirus into the host genome and latent persistence in long-lived cells throughout the body. Goats usually seroconvert in 2 to 8 weeks, but a long clinical latency (spanning years) is possible. Infected macrophages express viral proteins near major histocompatibility complex (MHC) antigens, which are recognized by T lymphocytes and stimulate cytokine production. 23,29 Disease results from inflammation elicited by the reaction of the immune system to the virus. CAEV often can be isolated from the synovial fluid and milk of infected animals. The virus is capable of making antigenic variants to help it evade the host immune response. At these target sites, CAEV induces chronic inflammation by invoking the host’s immune responses. The important target tissues of CAEV include the joints, mammary glands, lungs, and brain. Lymphocyte proliferation is a hallmark pathologic lesion seen in CAEV infection. Virus-infected macrophages may be more prone to activation and thereby induce proliferation of lymphocytes and macrophages. Initially the virus proliferates rapidly and induces a vigorous immune response that limits but does not eliminate the virus. The virus localizes in the macrophages of the synovium, lung, central nervous system, and mammary gland.
Proposed mechanisms for persistence include latent infection by a DNA provirus, viral replication that waits for monocytes to differentiate into macrophages in tissue, low levels of neutralizing antibodies, and viral mutation of env genes. “Restricted replication” allows the virus to remain latent in the host’s monocytes and undetected by the immune system. CAEV infects monocytes and macrophages and induces a persistent (lifelong) infection despite host antibody production. Pugh, in Sheep and Goat Medicine (Second Edition), 2012 PathogenesisĬAEV is a single-stranded ribonucleic acid (RNA) virus in the Lentivirus family that replicates by forming a reverse transcriptase–dependent deoxyribonucleic acid (DNA) intermediate that may become integrated into the host genome.
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