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PubMed2003

Heterodimerization of the two major envelope proteins is essential for arterivirus infectivity.

The two major envelope proteins of arteriviruses, the membrane protein (M) and the major glycoprotein (GP(5)), associate into a disulfide-linked heterodimer that is incorporated into the virion and has been assumed to be a prerequisite for virus assembly. Using an equine arteritis virus (EAV) infectious cDNA clone, we have analyzed the requirement for GP(5)-M heterodimerization and have identified the Cys residues involved in the formation of the GP(5)-M disulfide bond. The single Cys residue (Cys-8) in the M ectodomain was crucial for heterodimerization and virus infectivity. Mutagenesis of any of the five Cys residues in the GP(5) ectodomain or removal of the single GP(5) N-glycosylation site also rendered the full-length clone noninfectious. However, an analysis of revertants yielded an exceptional pseudorevertant in which residues 52 to 79 of the GP(5) ectodomain had been deleted and the original Cys-80-->Ser mutation had been maintained. Consequently, this revertant lacked the GP(5) N-glycosyation site (Asn-56) and retained only a single cysteine residue (Cys-34). By using this GP(5) deletion, we confirmed that Cys-34 of GP(5) and Cys-8 of M are essential for GP(5)-M heterodimerization, a key event in the assembly of the EAV envelope.

Amino Acid Sequence↗
PubMed2004

Porcine arterivirus infection of alveolar macrophages is mediated by sialic acid on the virus.

Recently, we showed that porcine sialoadhesin (pSn) mediates internalization of the arterivirus porcine reproductive and respiratory syndrome virus (PRRSV) in alveolar macrophages (Vanderheijden et al., J. Virol. 77:8207-8215, 2003). In rodents and humans, sialoadhesin, or Siglec-1, has been described as a macrophage-restricted molecule and to specifically bind sialic acid moieties. In the current study, we investigated whether pSn is a sialic acid binding protein and, whether so, whether this property is important for its function as a PRRSV receptor. Using untreated and neuraminidase-treated sheep erythrocytes, we showed that pSn binds sialic acid. Furthermore, pSn-specific monoclonal antibody 41D3, which blocks PRRSV infection, inhibited this interaction. PRRSV attachment to and infection of porcine alveolar macrophages (PAM) were both shown to be dependent on the presence of sialic acid on the virus: neuraminidase treatment of virus but not of PAM blocked infection and reduced attachment. Enzymatic removal of all N-linked glycans on the virus with N-glycosidase F reduced PRRSV infection, while exclusive removal of nonsialylated N-linked glycans of the high-mannose type with endoglycosidase H had no significant effect. Free sialyllactose and sialic acid containing (neo)glycoproteins reduced infection, while lactose and (neo)glycoproteins devoid of sialic acids had no significant effect. Studies with linkage-specific neuraminidases and lectins indicated that alpha2-3- and alpha2-6-linked sialic acids on the virion are important for PRRSV infection of PAM. From these results, we conclude that pSn is a sialic acid binding lectin and that interactions between sialic acid on the PRRS virion and pSn are essential for PRRSV infection of PAM.

Animals↗
PubMed2004

The immune response to equine arteritis virus: potential lessons for other arteriviruses.

The members of the family Arteriviridae, genus Arterivirus, include equine arteritis virus (EAV), porcine reproductive and respiratory syndrome virus (PRRSV), lactate dehydrogenase-elevating virus (LDV) of mice, and simian hemorrhagic fever virus (SHFV). PRRSV is the newest member of the family (first isolated in North America and Europe in the early 1990s), whereas the other three viruses were recognized earlier (EAV in 1953, LDV in 1960, and SHFV in 1964). Although arterivirus infections are strictly species-specific, the causative agents share many biological and molecular properties, including their virion morphology, replication strategy, unique properties of their structural proteins, and their ability to establish distinctive persistent infections in their natural hosts. The arteriviruses are each antigenically distinct and cause different disease syndromes in their natural hosts. Similarly, the mechanism(s) responsible for the prolonged and/or persistent infections that characterize infections with each arterivirus in their natural hosts are remarkably different. The objective of this review is to compare and contrast the immune response to EAV with that to the other three arteriviruses, and emphasize the potential relevance of apparent similarities and differences in the neutralization characteristics of each virus.

Animals↗
PubMed1998

Pathogenesis of coronavirus-induced infections. Review of pathological and immunological aspects.

Coronaviruses and arteriviruses infect multiple species of mammals, including humans, causing diseases that range from encephalitis to enteritis. Several of these viruses infect domestic animals and cause significant morbidity and mortality, leading to major economic losses. In this category are included such pathogens as transmissible gastroenteritis virus, porcine respiratory and reproductive virus and infectious bronchitis virus. The feline coronaviruses (FECV) generally do not cause infections with high morbidity but in a small percentage of cases, the virus mutates to become more virulent. This virus, feline infectious peritonitis virus (FIPV), causes severe disease in young cats. This disease is in large part immunopathological and understanding it is a major goal of coronavirus research.

Animals↗
PubMed1995

Interleukin-12 gene expression after viral infection in the mouse.

Interleukin-12 is a lymphokine that triggers gamma interferon secretion by various cells and differentiation of T-helper lymphocytes towards the Th1 subtype. Since viruses are potent inducers of gamma interferon production and elicit immune responses most probably mediated by Th1 cells, like B-cell immunoglobulin G2a secretion, we analyzed interleukin-12 message expression after infection of mice with lactate dehydrogenase-elevating virus, mouse hepatitis virus, and mouse adenovirus. Our results indicated that the message for the p40 component of interleukin-12 was transiently increased shortly after infection. Interleukin-12 was expressed mainly by macrophages. Therefore, production of interleukin-12 might constitute the initial event that would determine the subsequent characteristics of the immune response elicited by viral infections.

Adenoviridae Infections↗
PubMed2000

IFN-gamma-independent IgG2a production in mice infected with viruses and parasites.

After infection with some viruses and intracellular parasites, antibody production is restricted to IgG2a. We first observed that, whereas live viruses such as lactate dehydrogenase-elevating virus (LDV) or mouse adenovirus induced mostly an IgG2a response, a large proportion of antibodies produced against killed viruses were IgG1. This IgG1 antiviral response was suppressed when live virions were added to inactivated viral particles. These results indicate that the IgG2a preponderance is related to the infectious process itself rather than to the type of antigen involved. Since IFN-gamma is known to stimulate IgG2a production by activated B lymphocytes and to be secreted after infection, we examined the role of this cytokine in the antibody isotypic distribution caused by LDV. Most IgG2a responses were relatively unaffected in mice deficient for the IFN-gamma receptor or treated with anti-IFN-gamma antibody. A similar IFN-gamma-independent IgG2a secretion was observed after infection with the parasites Toxoplasma gondii and Trypanosoma cruzi. However, the IFN-gamma-independent IgG2a production triggered by infection still required the presence of functional T(h) lymphocytes. Therefore, signal(s) other than IFN-gamma secretion may explain the T(h)-dependent isotypic bias in antibody secretion triggered by viruses and parasites.

Adenoviridae↗
PubMed1994

Effect of infection by lactic dehydrogenase virus on expression of intercellular adhesion molecule-1 on vascular endothelial cells of pancreatic islets in streptozotocin-induced insulitis of CD-1 mice.

Streptozotocin (SZ)-induced insulitis, which is an animal model for insulin-dependent diabetes mellitus, was suppressed by lactic dehydrogenase virus (LDV) infection. There were no differences in degenerative and necrotic changes of islet cells between SZ-treated mice and SZ-treated mice with LDV infection during the pre-insulitis phase. The degree of insulitis was more severe and the plasma glucose levels were higher in SZ-treated mice than in SZ-treated mice with LDV infection. Severe degenerative and necrotic changes of cells with mononuclear cell infiltration into the islets were seen in the SZ-treated mice. Infiltration of these cells into islets was less in SZ-treated mice with LDV infection. During the pre-insulitis phase, there was slight expression of intercellular adhesion molecule-1 (ICAM-1) on the surface of vascular endothelial cells in and/or around islets in both groups. ICAM-1 expression on vascular endothelial cells increased in parallel to the degree of insulitis. The degree of this expression in SZ-treated mice was higher than in SZ-treated mice with LDV infection. These results suggest that expression of ICAM-1 on vascular endothelial cells in SZ-treated mice may be important for the development of insulitis. Also, decreased expression of ICAM-1 in the islets may be responsible for the inhibition of the development of insulitis seen in SZ-treated mice with LDV infection.

Animals↗
PubMed1993

Serological studies on the potential synergism of porcine reproductive and respiratory syndrome virus and influenza-, corona- and paramyxoviruses in the induction of respiratory symptoms in swine.

Sera from 265 finishing pigs belonging to 70 herds, in which severe respiratory disorders were observed, were examined for antibody prevalence to porcine reproductive and respiratory syndrome virus (PRRSV), influenza virus subtypes H3N2 and H1N1, porcine respiratory corona virus (PRCV) and a recently described porcine paramyxovirus (PPMV). By immunoperoxidase-monolayer assay 69.1% of these sera were positive for PRRSV. Hemagglutination inhibiting activity was found in 55.1% of the sera for influenza virus subtype H1N1 (strain A/swine/Arnsberg/1/81). in 51.3% for influenza virus subtype H3N2 (strain A/Hong Kong/1/68) and in 14.3% for PPMV. PRCV specific antibodies, as determined by differential competitive blocking enzyme-linked immunosorbent assay were demonstrated in 192 of 236 (81.3%) sera. In order to reveal associations interspecific coefficients were calculated for antibody prevalence between PRRSV and the other viruses. Positive associations to PRRSV titres were found to PRCV, PPMV and influenza virus subtype H1N1 titres. chi-square analysis showed the statistical significance of associations regarding PRCV and influenza virus subtype H1N1. Depletion of lung macrophages after PRRSV infection is discussed as a possible mechanism for the promotion of secondary infections.

Animals↗
PubMed1996

Dual infections of feeder pigs with porcine reproductive and respiratory syndrome virus followed by porcine respiratory coronavirus or swine influenza virus: a clinical and virological study.

Dual infections of pigs with porcine reproductive and respiratory syndrome virus (PRRSV) followed by a second common respiratory virus, either porcine respiratory coronavirus (PRCV) or swine influenza virus (SIV), were studied. The aim was to determine if dual infections, as compared to single virus infections, result in enhanced clinical manifestations. It was also examined if PRRSV replication affects replication of PRCV or SIV in the respiratory tract. Groups of conventional 10 week old pigs were inoculated with PRRSV-only (3 pigs), PRCV-only (4 pigs) or SIV-only (4 pigs). Dual inoculations with PRRSV-PRCV (4 pigs) and PRRSV-SIV (3 groups of 4, 4 and 5 pigs) were performed at a 3 day interval. A group of uninoculated control pigs (8 pigs) was included. The infection with PRRSV-only induced a transient fever (40.2 degrees C) at 2 DPI, but no respiratory signs. The PRCV-only infection remained subclinical. The SIV-only infection resulted in a one day fever (40.1 degrees C) with moderate tachypnoea and dyspnoea. Mean weight gain in the virus-inoculated groups was retarded compared with the control group. The PRRSV-PRCV infection induced a 9 day lasting fever (peak 40.9 degrees C) with tachypnoea, dyspnoea and productive coughing. The PRRSV-SIV infection resulted in fever and respiratory signs in all 3 groups. Clinical signs, however, were more pronounced in group 1 than in groups 2 and 3. Pigs of group 1 showed fever during 10 days (peak 41.4 degrees C), tachypnoea, marked dyspnoea with abdominal breathing, and a productive cough. Pigs of groups 2 and 3 had fever for 5 and 3 days (peaks 40.6 and 40.3 degrees C) respectively and mild respiratory disorders. Mean weight gain during 14 DPI of the 2nd virus was 5.9 kg in the PRRSV-PRCV group and 4.0, 6.8 and 6.7 kg in PRRSV-SIV groups 1, 2 and 3 respectively. Mean weight gain during the corresponding period in the PRRSV-only group was 8.6 kg. It was concluded that dual infections with viruses causes more severe disease and growth retardation than single PRRSV infection. PRCV excretion curves were similar in single and dual virus inoculated groups. Excretion of SIV was delayed by 2 days in the dual inoculated pigs. Thus, replication of the second virus is not (PRCV) or only slightly (SIV) affected by a prior infection with PRRSV.

Animals↗
PubMed1995

Pathogenesis of in utero infection in porcine fetuses with porcine reproductive and respiratory syndrome virus.

Porcine fetuses were exposed in utero to porcine reproductive and respiratory syndrome virus (PRRSV) at stages of gestation ranging from 34 to 85 days and examined 17 to 31 days later to determine the effect of gestational age on fetal susceptibility. For each of the 8 litters tested during the study, all of the fetuses of 1 horn of the uterus were exposed to virus by intraamniotic injection; those of the other horn were exposed similarly to a sham inoculum that consisted of sterile cell culture medium. Viral infectivity titers associated with fetal tissues collected at necropsy indicated that, regardless of gestational age, the virus had replicated in fetuses exposed intraamniotically. In addition, virus had also spread and replicated in sham-inoculated littermates in 3 litters. On the basis of these findings it appears that there may be little or no temporal difference in fetal susceptibility to infection with PRRSV. If so, the lack of early fetal death as a commonly recognized feature of naturally occurring cases of PRRS may be due to a greater resistance of early gestational fetuses to the lethal effects of PRRSV, as suggested by this study, and/or a greater likelihood of transplacental infection during late gestation.

Animals↗
PubMed1994

Difference in neutralization between lactate dehydrogenase-elevating virus isolated from acutely and chronically infected mice.

Mouse infection with lactate dehydrogenase-elevating virus (LDV) leads to lifelong viraemia, despite the production of neutralizing antiviral antibodies. To test whether viral persistence correlated with the development of resistance to these antibodies, we compared the neutralization of viral particles derived from acutely and chronically infected animals, using polyclonal and monoclonal anti-LDV antibodies. Whereas virus isolated during acute infection was efficiently neutralized, titres of LDV from chronically infected mice were only slightly reduced by antiviral antibodies. In addition, LDV from animals acutely infected with such poorly neutralizable virus from chronically infected mice was resistant to anti-LDV antibodies like their parental viral particles. These results suggest that LDV variants capable of escaping neutralization by antiviral antibodies can emerge in chronically infected animals.

Acute Disease↗
PubMed1996

Histopathological and immunofluorescent studies on transplacental infection in experimentally induced abortion by equine arteritis virus.

Five pregnant mares, at between 6 and 8 months gestation, were experimentally infected with the Bucyrus strain of equine arteritis virus (EAV). Of the five mares, four aborted and one died. The pathogenesis of the abortions was studied, using histopathologic techniques, tissue immunofluorescence and virus isolation. Common microscopic lesions in the maternal reproductive organs indicated myometritis with a degeneration of the myocytes and an infiltration of the mononuclear cells. Epithelial cells of the endometrial gland showed sporadic degeneration. Lesions in the fetal tissue included an atrophy of the lymphoid follicles in the spleen and lymph nodes with degenerated lymphocytes. The placentae were oedematous and degenerated fibroblasts were observed in the subvillous layers. Immunofluorescence detected EAV antigen in the myometrium and the endometrial gland in the dams, in the subvillous layer of the placentae, and in the aborted fetuses. EAV was recovered from the maternal uteri, placentae and fetuses. The placentae yielded the greatest amounts of the virus. Transplacental infection of the fetus was clearly demonstrated in the EAV infection.

Abortion, Veterinary↗
PubMed1994

Detection of equine arteritis virus following amplification of structural and nonstructural viral genes by reverse transcription-PCR.

A reverse transcription (RT)-PCR assay was developed for the detection of equine arteritis virus (EAV) in cell culture supernatant and in horse semen. Four different sets of oligonucleotide primers complementary to sequences located in the 3' end of the polymerase gene (open reading frame [ORF] 1b) and to sequences representing the entire ORFs 3, 4, and 7, which encode for nonstructural (ORFs 3 and 4) or viral nucleocapsid (ORF 7) proteins, were compared for their abilities to amplify the targeted EAV sequences by the RT-PCR procedure. The sensitivities of the RT-PCR for amplification of EAV sequences located in the 3' end of ORF 1b and ORF 4 were 2 median tissue culture infective doses (TCID50s) of viral particles in the EAV-infected cell culture supernatant for both ORFs and 20 and 200 TCID50s of viral particles, respectively, in virus-containing horse semen. The sensitivities were much lower when primers complementary to ORFs 3 and 7 were used in the RT-PCR, with a minimum detection limit of only 2 x 10(4) TCID50s of viral particles in virally infected cell culture supernatant, as determined by analyzing the resulting RT-PCR products on ethidium bromide-stained agarose gels. The specificities of the RT-PCR assays for all primer sets tested were confirmed when the amplified cDNA products of the expected size reacted positively with the corresponding virus-specific digoxigenin-labeled cDNA probes in the chemiluminescence assays. Although the sensitivity of the RT-PCR for amplification of ORF 3 and 7 sequences was lower, all sets or primers were capable of amplifying several cell culture-adapted EAV field isolates when the virus was present in high enough quanities in the test sample. When horse semen samples were analyzed for the presence of EAV by the RT-PCR with primers specific to the ORF 1b 3' end and ORF 4 sequences and by virus isolation in cell cultures, there was 100% concordance among the assays. The RT-PCR assay targeting the 3' end of ORF 1b and/or ORF 4 EAV RNA may be an alternative to conventional methods for the diagnosis of EAV infection in horses.

Animals↗
PubMed1994

Nitric oxide production by splenic macrophages is not responsible for T cell suppression during acute infection with lactate dehydrogenase-elevating virus.

Cellular immune responses of mice are transiently suppressed during acute infection with lactate dehydrogenase-elevating virus (LDV). Immunosuppression of mice correlated with a greatly impaired in vitro proliferative response of the majority of the T cells to Con A or anti-CD3 Abs, which could not be reversed by the addition of rIL-2. We have examined whether the T cell suppression is caused by nitric oxide (NO) produced by activated macrophages, which are observed in acutely infected mice. Spleen macrophages from 3-day LDV-infected mice exhibited a 6- to 10-fold increased potential for producing NO, measured as nitrite or nitrite plus nitrate in the culture fluid, but produced significant amounts of NO in vitro only when incubated with IFN-gamma produced by Con A-stimulated T cells in the spleen cell population. Furthermore, we found that the concentrations of NO produced by macrophages in cultures of spleen cells from LDV-infected mice in the presence of IFN-gamma were insufficient to cause a reduction in the proliferative response of T cells in the spleen cell population. An excess of activated macrophages had to be added to achieve T cell suppression. NO inhibition of Con A-induced T cell proliferation exhibited a very sharp dose-response curve. In one experiment little suppression was observed at NO concentrations equivalent to 12 microM nitrite and below, whereas almost complete inhibition was observed at twice the NO concentration. We conclude that NO is not responsible for T cell suppression in LDV-infected mice.

Animals↗
PubMed1996

Stability of porcine reproductive and respiratory syndrome virus in the presence of fomites commonly found on farms.

OBJECTIVE: To determine the survival of porcine reproductive and respiratory syndrome virus (PRRSV) on nonliving substances (fomites) at 25 to 27 C. DESIGN: Prospective controlled study. SAMPLE POPULATION: 3 solid, 6 porous, and 7 liquid fomites. PROCEDURE: The fomites were contaminated with known concentrations of PRRSV. Samples for virus isolation were obtained on day 0 through day 11, assayed in cell cultures, and stained with fluorescent antibody conjugate. RESULTS: The virus was recovered only on day-0 samples of alfalfa, wood shavings, straw, plastic, boot rubber, and stainless steel. Virus was isolated from city water through day 11, from well water through day 9, and from 2 buffer solutions for 4 and 6 days. The virus was isolated only on day 0 from swine saliva, urine, and fecal slurry. CLINICAL IMPLICATIONS: Results indicated that PRRSV is a fairly labile virus, but because of its duration of viability in water, contamination of drinking water and lagoons by PRRSV-shedding swine would serve as sources of virus to infect susceptible swine.

Animal Feed↗
PubMed1997

Failure to establish chronic infection of the reproductive tract of the male horse with a South African asinine strain of equine arteritis virus (EAV).

Eight sexually mature horse stallions were inoculated intranasally with a South African asinine strain of EAV, a strain that was isolated from the semen of a donkey carrier. All horses developed fever, with maximum rectal temperatures of 38.9-39.9 degrees C recorded 3-6 d post challenge. Six horses showed very mild clinical signs of equine viral arteritis and two were asymptomatic. The virus was recovered from the nasopharynxes of six horses 2-7 d after inoculation, and from buffy-coat samples of all horses, 2-11 d after inoculation. Seroconversion to EAV was detected on days 8 and 10 and peak serum-virus-neutralizing antibody titres ranging from log10 1.2-1.8, on days 14-20 after challenge. The titres varied from log10 0.9-1.2 after about 10 weeks, when the experiment was terminated. In three stallions euthanased on days 5, 7 and 9 after challenge, virus was detected inconsistently in different parts of the reproductive tract and urine. No virus was isolated from the tissues of the reproductive tract collected from stallions on days 16, 23 and 68 after challenge. Five stallions were bred to six seronegative mares between 13 and 34 d post challenge. No clinical signs of EAV were observed, and neither was seroconversion detected in any of the mares after mating. No virus was recovered from semen samples collected at the time of breeding. The results of this study demonstrated that the tissues of the reproductive tracts of the stallions did not become persistently infected with a South African asinine strain of EAV.

Animals↗
PubMed1998

The neutralization epitope of lactate dehydrogenase-elevating virus is located on the short ectodomain of the primary envelope glycoprotein.

We have measured by indirect ELISA the binding of neutralizing and non-neutralizing anti-lactate dehydrogenase-elevating virus (LDV) polyclonal and monoclonal antibodies to synthetic peptides representing unmodified hydrophilic segments of LDV proteins. Using this method a single neutralization epitope has been shown to be located in the very short (about 30 amino acid long) ectodomain of the primary envelope glycoprotein, VP-3P, encoded by ORF 5. Although the neutralization epitopes of neuropathogenic and non-neuropathogenic LDVs differ slightly in amino acid sequences, the neutralizing antibodies bind strongly to the epitopes of both groups of viruses. However, the neutralization epitopes of neuropathogenic and non-neuropathogenic LDVs are associated with different numbers of polylactosaminoglycan chains (1 and 3, respectively) which may affect the binding of neutralizing antibodies to the virions of these LDVs. The ELISA using synthetic peptides containing the neutralization epitope provides a novel, rapid, sensitive, and inexpensive method for quantitating LDV neutralizing antibodies in infected mice.

Amino Acid Sequence↗
PubMed2003

Lactic dehydrogenase virus infection reduces the expulsion of the nematode Nippostrongylus brasiliensis.

The interleukin (IL)-13-mediated goblet cell response is the major host effector system involved in the expulsion of Nippostrongylus brasiliensis. Lactic dehydrogenase virus (LDV) induced higher levels of N. brasiliensis egg production compared with controls, but the effect of LDV infection on worm expulsion of, and goblet cell and IL-13 responses to, N. brasiliensis have not been studied. In this study, the effects of LDV infection on these host responses against N. brasiliensis were examined. Mice with chronic LDV infection showed significantly lower worm expulsion rates than non-LDV-infected mice after N. brasiliensis infection, and there were no significant differences in the ratio of female versus male adult worms between control and LDV-infected mice. The number of goblet cells in LDV-infected mice was significantly lower than that in controls. In addition, the levels of IL-13 gene expression in lymph nodes were significantly lower in LDV-infected mice compared with controls. These results suggest that LDV infection reduces the protective immune responses against N. brasiliensis infection by the suppression of IL-13 production.

Animals↗