Modulation of lethal and persistent rat parvovirus infection by antibody

Gaertner, Diane J.; Jacoby, Robert O.; Paturzo, Frank X.; Johnson, Elizabeth A.; Brandsma, Janet L.; Smith, Abigail L.

doi:10.1007/bf01311299

Cited by 13 publications

(3 citation statements)

References 10 publications

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“…The variability with which RV was recovered, especially at long intervals after inoculation of pups, coupled with the detection only of 1.3 and 0.8 kbp DNA bands in these seropositive rats, is consistent with potential restriction of RV expression by antibody. In addition, persistently infected athymic pups, which make little or no antibody to RV, harbor RV DNA typical of RF virus rather than DNA bands observed in persistently infected, seropositive euthymic pups [15].…”

Section: Discussionmentioning

confidence: 92%

Persistent rat parvovirus infection in individually housed rats

Jacoby

Johnson

Paturzo

et al. 1991

Archives of Virology

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The duration of infection with rat virus (RV), an autonomous rodent parvovirus, was examined at multiple intervals over 6 months in rats inoculated by the oronasal route at 2 days of age or 4 weeks of age and individually housed after weaning to prevent cross-infection. Infectious virus was recovered by explant culture from 32 of 80 rats inoculated as pups and was detected as late as 6 months after inoculation. Rats inoculated as juveniles developed acute infection, but virus was not detected beyond 7 weeks after inoculation. Tissues from rats in both age groups were surveyed for RV DNA by Southern blotting using a double-stranded DNA probe made from a 1700 bp cloned fragment of RV spanning map units 0.19-0.52. Band patterns representative of acute infection (juvenile rats) were consistent with the replicating form of RV DNA, whereas patterns representative of persistent infection (rats inoculated as pups) were suggestive of defective or non-productive viral replication.

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Section: Discussionmentioning

confidence: 92%

Persistent rat parvovirus infection in individually housed rats

Jacoby

Johnson

Paturzo

et al. 1991

Archives of Virology

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“…By contrast, Virelizier (51) and subsequently ourselves (41) found that antibody treatment could cure influenza virus pneumonia in immunodeficient mice. Antibody treatments have reportedly also cured other viral diseases in immunodeficient mice, such as Sindbis virus infection of the central nervous system in severe combined immunodeficiency (SCID) mice (33), Theiler's murine encephalomyelitis virus infection in athymic mice (15), and parvovirus infection in athymic newborn rats (17). In addition, treatment with a singularly effective monoclonal antibody (MAb) but not with an antiserum cured a herpes simplex virus infection of the vaginal mucous membranes in Tcell-depleted mice (14), although passive antibody often only delayed morbidity in this infection (28,37,47,55).…”

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confidence: 99%

Virus-neutralizing antibodies of immunoglobulin G (IgG) but not of IgM or IgA isotypes can cure influenza virus pneumonia in SCID mice

Palladino

Mozdzanowska

Washko

et al. 1995

J Virol

180

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The ability of monoclonal antibodies (MAbs) to passively cure an influenza virus pneumonia in the absence of endogenous T-and B-cell responses was investigated by treating C.B-17 mice, homozygous for the severe combined immunodeficiency (SCID) mutation, with individual monoclonal antiviral antibodies 1 day after pulmonary infection with influenza virus PR8 [A/PR/8/34(H1N1)]. Less than 10% of untreated SCID mice survived the infection. By contrast, 100% of infected SCID mice that had been treated with a single intraperitoneal inoculation of at least 175 g of a pool of virus-neutralizing (VN ؉) antihemagglutinin (anti-HA) MAbs survived, even if antibody treatment was delayed up to 7 days after infection. The use of individual MAbs showed that recovery could be achieved by VN ؉ anti-HA MAbs of the immunoglobulin G1 (IgG1), IgG2a, IgG2b, and IgG3 isotypes but not by VN ؉ anti-HA MAbs of the IgA and IgM isotypes, even if the latter were used in a chronic treatment protocol to compensate for their shorter half-lives in vivo. Both IgA and IgM, although ineffective therapeutically, protected against infection when given prophylactically, i.e., before exposure to virus. An Fc␥-specific effector mechanism was not an absolute requirement for antibody-mediated recovery, as F(ab) 2 preparations of IgGs could cure the disease, although with lesser efficacy, than intact IgG. An anti-M2 MAb of the IgG1 isotype, which was VN ؊ but bound well to infected cells and inhibited virus growth in vitro, failed to cure. These observations are consistent with the idea that MAbs of the IgG isotype cure the disease by neutralizing all progeny virus until all productively infected host cells have died. VN ؉ MAbs of the IgA and IgM isotypes may be ineffective therapeutically because they do not have sufficient access to all tissue sites in which virus is produced during influenza virus pneumonia.

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“…Additionally, transfer of colostral or serum antibodies before or at the time of infection protected infant rats from developing RV infection. In contrast, administration of immune sera to infant rats 1 day after virus inoculation failed to prevent RV infection (11). Furthermore, rats inoculated at 6 days of age develop high anti-RV antibody titers, and yet virus is able to persist (15).…”

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confidence: 93%

Immune Responses to the Major Capsid Protein during Parvovirus Infection of Rats

Ball-Goodrich

Paturzo

Johnson

et al. 2002

J Virol

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Rat virus (RV) is a common parvovirus of laboratory rodents which can disrupt rat-based research. Prenatal or perinatal infection can be pathogenic or lead to persistent infection, whereas infection of adult rats is typically self-limiting. Effects on the host immune system have been documented during RV infection, but little is known about immune responses necessary for viral clearance. Our studies were conducted to identify humoral and cellular responses to the predominant capsid protein, VP2, during experimental infection of adult rats. We observed VP2-specific proliferation, gamma interferon production, and an immunoglobulin G2a humoral response that is maintained for at least 35 days following RV infection. These results strongly suggest the induction of virus-specific Th1-mediated immunity.Parvoviruses are nonenveloped viruses with a singlestranded genome of approximately 5 kb. Viral replication is dependent on many cellular functions, particularly those expressed during S phase of the cell cycle (7). Rodent parvoviruses encode two classes of proteins: nonstructural (NS) proteins and structural or capsid proteins (VP). NS proteins are involved in viral replication, transcription, and cytotoxicity. VP1 comprises 15% of the icosahedral virion, and its coding sequence contains all of VP2 plus 140 additional N-terminal amino acids. VP2 is the predominant capsid protein, accounting for approximately 85% of the virion. VP3, a cleavage product of VP2, is present in small, varying amounts in DNAcontaining virions.A recent national survey found that parvovirus infections are highly prevalent among laboratory rats and mice (17). Infection with some of these agents can be lethal in fetal or perinatal animals, probably due to high numbers of mitotically active cells that serve as targets for cytolytic viral replication. Larger impacts on biomedical research result from clinically silent infections in infant or adult rodents in which biological processes and immune responses are altered. Specifically, infections with murine parvoviruses such as mouse minute virus and mouse parvovirus are known to inhibit several T-cell effector functions in vitro (2, 8); suppress antigen-induced proliferation of specific cloned T cells (18); augment the rate of tumor, allogeneic, and syngeneic graft rejection; and modulate other T-cell effector functions (19,21). In addition, infection with rat virus (RV), the prototypic parvovirus of rats, can decrease lymphocyte viability and suppress proliferative responses to alloantigens (4), diminish responses of mixed lymphocyte culture and cytolytic T cells from peripheral and mesenteric lymph nodes (20), alter humoral responses to ovalbumin (5), and provoke autoimmune diabetes in the diabetes-resistant strain of Biobreeding/Worcester (BB/WOR) rats (3,5,13).Despite the impact of these agents on host immunity, little is known about immune responses to rodent parvoviruses. It is known that rats develop antiviral antibodies and perivascular mononuclear cell infiltrates in infected tissues (10,14)....

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Modulation of lethal and persistent rat parvovirus infection by antibody

Cited by 13 publications

References 10 publications

Persistent rat parvovirus infection in individually housed rats

Persistent rat parvovirus infection in individually housed rats

Virus-neutralizing antibodies of immunoglobulin G (IgG) but not of IgM or IgA isotypes can cure influenza virus pneumonia in SCID mice

Immune Responses to the Major Capsid Protein during Parvovirus Infection of Rats

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