Lactate Dehydrogenase-Elevating Virus: Biology and Pathogenesis

Polyclonal B Cell Activation of IgG2a and IgG2b Production by Infection of Mice with Lactate Dehydrogenase-Elevating Virus Is Partly Dependent on CD4+Lymphocytes

“…One working hypothesis that may explain the IgG2a-restricted polyclonal activation of B cells by LDV infection might be as follows: Replication of LDV in the subpopulation of permissive macrophages probably results in the release of a variety of lymphokines, which may affect T cell functions, but only the production of IFNoc/ß has been documented so far (23,50). At the same time phagocytosis of LDV and of permissive macrophages that are killed by LDV infection (38,51) probably results in the processing of LDV proteins and presentation to TH cells, which in turn stimulates the anti-LDV antibody response by B lymphocytes.…”

Experimental Porcine Reproductive and Respiratory Syndrome Virus Infection in One-, Four-, and 10-Week-Old Pigs

“…Lactate dehydrogenase-elevating virus infection also induces antibodies that are not protective early in the course of the disease, but this is not a feature of SHF and EAV infection. 7,20 A comparison of clinical signs and hematologic changes associated with PRRSV with those associated with related viruses reveals similarities to SHF virus, EAV, and LDEV.…”

“…Nasal, fecal, and conjunctival swabs and clotted and heparinized blood were collected on the day before exposure and on days 1,4,7,14,21, and 28 PE for virus isolation (swabs, buffy coat, serum, and plasma), PRRS serum antibody determination, and complete blood counts. g Tissues and urine for virus isolation and tissue for histopathology were collected at necropsy on days 7 and 28 PE.…”

“…The mean body temperature in the principal l-week-old pigs was elevated as compared with that of the controls on days 3,[5][6][7][8][9][10][11][12][13][14]16, and 18 PE (P < 0.05). There was an increase in the frequency of sneezing in the principal pigs during days 6-l2 PE.…”

Lactate Dehydrogenase-Elevating Virus, Equine Arteritis Virus, and Simian Hemorrhagic Fever Virus: A New Group of Positive-Strand RNA Viruses

“…LDV has attracted considerable attention as a research model because of (1) its unique restricted host specificity for a subpopulation of rnacrophages, (2) the lifelong persistent infection it invariably establishes in all mouse strains, which is asymptomatic except for subtle effects on the host immune system, and (3) its ability to cause under a multifactorial setting a generally fatal motor neuron disease (age-dependent poliomyelitis, ADPM) in certain mouse strains. General aspects of LDV research have been covered in several previous reviews Mahy, 1975, 1985;Brinton, 1980Brinton, ,1982Brinton, ,1986Cafruny, 1989). General aspects of LDV research have been covered in several previous reviews Mahy, 1975, 1985;Brinton, 1980Brinton, ,1982Brinton, ,1986Cafruny, 1989).…”