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PubMed2005

Platelet function and association of bovine viral diarrhea virus with platelets of persistently infected cattle.

OBJECTIVE: To determine whether viral involvement with platelets obtained from cattle persistently infected (PI) with bovine viral diarrhea virus (BVDV) is associated with altered platelet function or decreased platelet counts. SAMPLE POPULATION: Platelets obtained from 8 cattle PI with BVDV and 6 age-, sex-, and breed-matched uninfected control cattle. PROCEDURE: Manual platelet counts were determined, and platelet function was assessed through optical aggregometry by use of the aggregation agonists ADP and platelet-activating factor. Identification of BVDV in serum and preparations of purified platelets was determined by use of virus isolation tests. RESULTS: No significant difference in platelet counts was detected between cattle PI with BVDV and control cattle. In response to the aggregation agonists, maximum aggregation percentage and slope of the aggregation curve were not significantly different between cattle PI with BVDV and control cattle. We isolated BVDV from serum of all PI cattle and from purified platelets of 6 of 8 PI cattle, but BVDV was not isolated from serum or platelets of control cattle. CONCLUSIONS AND CLINICAL RELEVANCE: Isolation of BVDV from platelets in the peripheral circulation of cattle immunotolerant to BVDV does not result in altered platelet function or decreases in platelet counts.

Animals↗
PubMed1982

Characterization of a cell culture persistently infected with the DA strain of Theiler's murine encephalomyelitis virus.

We established a persistent infection in L 929 cells with the DA strain of Theiler's murine encephalomyelitis virus. Our studies showed that only a small number of cells in the cultures contained infectious virus or viral antigen. A role for interferon in the maintenance of persistence was suggested. Viral isolates from the cultures were not temperature sensitive, nor did they contain viral capsid polypeptide mutations or defective interfering particles. T1 oligonucleotide maps showed evidence of mutation in two of three isolates.

Animals↗
PubMed2006

The BZLF1 homolog of an Epstein-Barr-related gamma-herpesvirus is a frequent target of the CTL response in persistently infected rhesus macaques.

Although CD8(+) T lymphocytes targeting lytic infection proteins dominate the immune response to acute and persistent EBV infection, their role in immune control of EBV replication is not known. Rhesus lymphocryptovirus (rhLCV) is a gamma-herpesvirus closely related to EBV, which establishes persistent infection in rhesus macaques. In this study, we investigated cellular immune responses to the rhLCV BZLF1 (rhBZLF1) homolog in a cohort of rhLCV-seropositive rhesus macaques. rhBZLF1-specific IFN-gamma ELISPOT responses ranging between 56 and 3070 spot-forming cells/10(6) PBMC were detected in 36 of 57 (63%) rhesus macaques and were largely mediated by CD8(+) T lymphocytes. The prevalence and magnitude of ELISPOT responses were greater in adult (5-15 years of age) rather than juvenile macaques (<5 years of age), suggesting that rhBZLF1-specific CTL increase over time following early primary infection. A highly immunogenic region in the carboxyl terminus of the rhBZLF1 protein containing overlapping CTL epitopes restricted by Mamu-A*01 and other as yet unidentified MHC class I alleles was identified. The presence of a robust CD8(+) T lymphocyte response targeting this lytic infection protein in both rhesus macaques and humans suggests that these CTL may be important for immune control of EBV-related gamma-herpesvirus infection. These data underscore the utility of the rhLCV-macaque model for studies of EBV pathogenesis.

Amino Acid Sequence↗
PubMed2006

Establishment of functional B cell memory against parvovirus B19 capsid proteins may be associated with resolution of persistent infection.

Parvovirus B19 (B19) infection can occur during acute lymphoblastic leukemia and persistent viral infection can occur despite intravenous immunoglobulin administration. Here, evidence is presented that resolution of persistent B19 infection in an acute lymphoblastic leukemia patient may be associated with the simultaneous strengthening of antigen-specific B cell memory against the B19 capsid protein VP2 and diminution in the memory response against the B19 non-structural protein 1 (NS1). Determination of antigen-specific B cell memory status may enhance the serological and molecular analyses of persistent B19 infection.

B-Lymphocytes↗
PubMed1998

The immune response of cattle, persistently infected with noncytopathic BVDV, after superinfection with antigenically semi-homologous cytopathic BVDV.

Cattle persistently infected (PI) with noncytopathic (ncp) bovine virus diarrhea virus (BVDV) are at risk for developing fatal mucosal disease (MD), which is considered to occur after superinfection with antigenically homologous cytopathic (cp) BVDV. In this study, we intranasally inoculated four PI-animals, that were PI with 2 ncp BVDV strains with 10(5) TCID50 antigenically closely related cp BVDV. Two PI-animals were inoculated with 10(5) TCID50 ncp BVDV and one PI-animal, with virus free cell culture medium. Two out of four PI-animals that were inoculated with cp BVDV, developed MD and were euthanized at day 17 and at day 24 after infection. Postmortem, both animals showed typical lesions of MD and cp BVDV was isolated. The other two PI-animals that were inoculated with cp BVDV did not develop MD and were euthanized at day 51. They showed ulcerations in the gastrointestinal tract, cp BVDV was isolated and neutralizing antibodies were detected. From the three PI-animals, that were inoculated with ncp BVDV or cell culture medium, cp BVDV was also isolated. Cross neutralization tests were performed and no antigenic differences could be detected between the cp strains isolated from the PI-animals. Lymphocyte subsets of these PI-animals were determined by flow cytometric analysis. Before superinfection, the percentages of gamma delta subsets were much higher in the PI-animals that did not develop MD than in nonviremic control animals and in the PI-animals that died of MD. From this study we conclude that the presence of antigenically closely related cp BVDV in PI-animals does not necessarily lead to the development of MD and that besides the antigenic relatedness between the persisting ncp BVDV and cp BVDV other factors, for instance the number of circulating gamma delta cells, might determine whether or not PI-animals develop MD.

Animals↗
PubMed1994

Virus-like particles in MDCK cells persistently infected with Borna disease virus.

A line of Madin Darby canine kidney (MDCK) cells persistently infected with Borna disease virus was examined by electron microscopy. Thin sections revealed the presence of intracytoplasmic virus-like particles ranging from 50-100 nm in diameter. Nuclei of the infected cells exhibited accumulation of electron-dense granular structures 15-18 nm in diameter. The intracytoplasmic particles were roughly spherical with a limiting membrane, suggesting the presence of a lipid-containing envelope. The internal structure consisted of strand-like material which in some cases was condensed underneath the envelope. The possible relationship of these particles to Borna disease virions is discussed.

Animals↗
PubMed1975

Iterferon induction in mice by BHK cells persistently infected with HVJ.

Intraperitoneal injection into mice of BHK-HVJ cells (BHK cells persistently infected with HVJ) induced considerable amounts of circulating interferon. Sonication of BHK-HVJ cells almost totally abolished their interferon inducing capacities. This result suggests that a certain native organized structure of virus infected cells might be essential for production of interferon in this system, as is suggested in the in vitro sytem.

Animals↗
PubMed1979

Growth phase related loss of measles virus surface-associated antigens and cytotoxic susceptibility in persistently infected cells.

Fluctuations in the expression of measles virus surface-associated antigens in persistently infected human Lu 106 cells were analysed by the use of human sera which preferentially reacted with the haemolysin or haemagglutinin component. The variations observed correlated with the proportion of cells expressing surface-antigen, as examined in population analysis by indirect immunofluorescence, a radio-labelled antiglobulin technique and a cytotoxicity assay. Microfluorometric analysis revealed no changes in antigen expression at the single-cell level. The number of cells that were positive by immunofluorescence among exponentially growing, low density cells remained relatively constant. These cells were more susceptible to cytotoxicity mediated by both antisera and complement than cells seeded at high density and kept in the stationary phase. The percentage of fluorescent cells among the latter cells gradually decreased. Thus cytotoxic susceptibility was related to the proportion of the total cell population that was antigen-bearing, rather than to variations in the expression of antigen at the single-cell level. In mitotic cells, polarization of antigen, as measured by indirect immunofluorescence of pre-fixed cells, was frequently seen. Often only one of the daughter cells expressed surface antigen. The results imply that cells in stationary phase may lose antigen from their surface, possibly by shedding, and furthermore that re-expression would demand a new cell cycle.

Antigens, Surface↗
PubMed1985

Enhanced intranuclear expression of measles virus following exposure of persistently infected cells to cyclic AMP.

The intracellular distribution of measles virus inclusion bodies in persistently infected human cells (AV3A1/MV) changed markedly following continuous exposure to 3', 5' cyclic adenosine monophosphate (cAMP). When assayed by immunofluorescence, the number of cells with intranuclear virus inclusions increased from 5 to 10% to 80 to 90% after exposure to 1 mM-cAMP for 4 days. Exposure of cells to cAMP also resulted in a twofold increase in the average number of inclusions in invaded nuclei. Similar but less pronounced changes occurred in cells treated with inducers of adenylate cyclase and an inhibitor of phosphodiesterase. Examination of cAMP-treated cells by electron microscopy indicated that viral inclusion bodies consisted of typical helical nucleocapsids. No evidence of nucleocapsids crossing the nuclear membrane (through nuclear pores) was found.

Adenylyl Cyclases↗
PubMed2006

Lymphocytic choriomeningitis virus mx strain does not induce the expression of tumor-associated carbonic anhydrase IX in persistently infected HeLa cells.

Summary. - Lymphocytic choriomeningitis virus (LCMV) is an arenavirus that readily causes persistent infections, in which it does not interfere with vital functions of the cells, but can affect expression of "luxurious" genes. MX strain of LCMV (MX LCMV) has been identified as an agent transmissible by cell-to-cell contact in the human carcinoma MaTu cells grown in a mixed culture with HeLa cells. When compared to uninfected HeLa, the MaTu-MX-infected HeLa cells, to which the virus was transmitted via co-cultivation with mitomycin C-treated MaTu cells, showed an elevated expression of a protein called MN, suggesting that MN can be induced by MX LCMV. MN protein was later identified as the carbonic anhydrase isoform IX (CA IX), whose expression has been predominantly associated with hypoxic tumors of poor prognosis. Since the proposal that MX LCMV can induce such a cancer-related protein could substantially change our view on the biology of LCMV-host interaction we undertook its verification. Instead of co-cultivation, we used MaTu cell-free extracts to transmit MX LCMV to HeLa cells. These cells were then grown for more than 30 passages, but the level of MN/CA IX did not increase throughout the whole cultivation period as compared to uninfected HeLa cells. Moreover, a treatment of MaTu-MX-infected HeLa cells with ribavirin eliminated the virus, but did not reduce the MN/CA IX expression. Our results clearly showed that MN/CA IX is independent of MX LCMV and that the virus itself does not influence the MN/CA IX level in HeLa cells.

Antigens, Neoplasm↗
PubMed1980

Persistent infection of mouse tumor cells with mumps virus.

A mouse tumor cell line (MCT) persistently infected with mumps virus (strain Urabe) was obtained. No antibody or chemicals were required for establishment or maintenance of the infected cell line (M-MCT). No difference was observed by light microscopy between MCT and M-MCT cells, except for cytoplasmic inclusion bodies in 10--20% of the M-MCT cells. Hemadsorption of chicken erythrocytes, which did not necessarily coincide with inclusion positive cells was shown by 10--20% of the M-MCT cells. Immunofluorescence staining revealed that almost all M-MCT cells contained mumps virus antigens, which were seen mainly in the cytoplasm as fine granules, dots, or large clumps. Infectious mumps virus was consistently detected in the culture fluid and the released virus showed some temperature sensitivity when assayed at 34 degrees C and 40 degrees C. M-MCT was resistant to superinfection with homologous virus and showed some resistance to heterologous viruses. Thirty one clones of M-MCT were isolated by the soft agar method. Some, but not all, clones had viral antigen and all those with antigen released virus into the culture medium. The growth rates of MCT and M-MCT cells as monolayer cultures in vitro were similar, but the transplantability of M-MCT cells in syngeneic C57BL/6 mice was lower than that of MCT cells.

Animals↗
PubMed1987

Long-term persistent infection of macaque monkeys with the simian immunodeficiency virus.

Juvenile rhesus macaques 6 to 18 months of age were experimentally infected by intravenous inoculation with the simian immunodeficiency virus (SIV), the T cell-tropic retrovirus of monkeys related to the human acquired immunodeficiency syndrome (AIDS) virus HIV. The SIV used for inoculation was grown either in normal human peripheral blood lymphocytes in the presence of interleukin 2 or in the human tumour cell line HUT-78. Eight of the macaques died 129 to 352 days post-inoculation with a variety of clinical and pathological findings paralleling those of AIDS in humans. However eight other animals became persistently infected for prolonged periods; these eight macaques remained alive at 537 and 820 days post-inoculation despite persistent lymphadenopathy and our continued ability to isolate SIV. The ability of these monkeys to survive infection correlated directly with the strength of their antibody response to SIV. Infection was also established in macaques using approximately 100 tissue culture infectious doses of HUT-78-grown SIV. There was no correlation between the dose of virus inoculum and either the strength of the antibody response or clinical outcome. These results demonstrate that SIV infection of macaques can be used not only to study acute AIDS but also to mimic the long-term persistent infection seen in carriers of HIV.

Acquired Immunodeficiency Syndrome↗
PubMed2002

Restriction of poliovirus RNA replication in persistently infected nerve cells.

The aetiology of post-polio syndrome may involve persistence of poliovirus (PV) in the CNS. PV persists in the CNS of infected paralysed mice for over a year after the acute phase of paralytic poliomyelitis. However, infectious PV particles cannot be recovered from homogenates of CNS from paralysed mice after the acute phase of disease, indicating that PV replication is restricted. To identify the molecular mechanism by which PV replication is limited, PV RNA synthesis was analysed by estimating the relative level of genomic (plus-strand) and complementary (minus-strand) PV RNA in the CNS of persistently infected mice. PV RNA replication decreased during the 6 months following onset of paralysis, due mainly to inhibition of plus-strand RNA synthesis. Thus, restriction of PV RNA synthesis may contribute to persistence by limiting virus replication in the mouse CNS. Interestingly, viral RNA replication was similarly inhibited in neuroblastoma IMR-32 cell cultures persistently infected with PV. This in vitro model thus shows that cellular factors play a role in the inhibition of viral RNA synthesis.

Animals↗
PubMed1981

An intracellular interaction between a temperature-sensitive mutant and the original wild-type HVJ (sendai virus) is responsible for the establishment and maintenance of HVJ persistent infection.

In order to understand the selective survival of temperature-sensitive (ts) mutants in persistent infection by HVJ (Sendai virus), an intracellular interaction between a ts clone (HVJ cl.14) isolated from HVJ carrier G2 cells and the original wild-type virus (HVJo) was studied. HVJ cl.14 differed from HVJo mainly in its ts property at 39 degrees C, weak cytopathogenicity and faster electrophoretic mobility of P protein (P77K), but showed similar trypsin-activated growth to that of HVJo. When LLCMK2 cells were simultaneously infected with HVJo and HVJ cl.14 at 32 degrees C, synthesis of HVJo-derived P protein (P79K) was inhibited with concomitant reduction of cytopathic effect (c.p.e.) and more dominant growth of HVJ cl.14 was observed. For the analysis of progeny viruses in these mixed infections, another mutant of HVJo designated HVJe which formed plaques activated only by elastase was isolated and employed instead of HVJo. At 39 degrees C, HVJ cl.14 was rescued by coinfected HVJe at about 900- to 13 000-fold over single infection. This recovery was also shown by sequential synthesis of HVJ cl.14-derived P protein (P77K) following the earlier synthesis of HVJo-derived P polypeptide (P79K) in the mixed infection at 39 degrees C. However, the u.v. inactivation of HVJe or HVJ cl.14 resulted in a loss of their activity on rescue or on c.p.e. reduction, suggesting the necessity of protein synthesis by opposite viruses for these interactions. The mechanisms involved in the predominant growth of the ts mutant and concomitant reduction of c.p.e. seemed to provide a general explanation for the preferable persistence of the ts mutant in the HVJ carrier cells.

Cell Line↗
PubMed1991

Loss of the endothelin signal pathway in C6 rat glioma cells persistently infected with measles virus.

Endothelin 1 causes a strong Ca2+ signal in C6 rat glioma cells as measured by fura-2 fluorescence. This endothelin 1-induced Ca2+ signal was not observed when the cells were persistently infected with a measles virus strain of subacute sclerosing panencephalitis (SSPE, strain Lec). Binding of 125I-labeled endothelin 1 to the C6/SSPE cells was less than 5% of the binding to the C6 control cells, suggesting that the impairment in signal transduction was due to a loss of binding sites for endothelin 1. Treatment of the C6/SSPE cells with measles antiserum resulted in the loss of expression of viral proteins located in the membrane as well as inside the cells (antigenic modulation), but it restored neither the endothelin 1-induced Ca2+ rise nor the 125I-endothelin 1 binding. Cocultivation of uninfected C6 cells with C6/SSPE cells (9:1 ratio) resulting in contact-mediated transmission of measles virus showed that the 125I-endothelin 1 binding activity was gradually lost as a consequence of persistent virus infection.

Animals↗
PubMed1999

Persistent infection of bovine herpesvirus type 4 in bovine endothelial cell cultures.

Herpesviruses can establish a persistent infection in the cells and tissues of their natural hosts and thus may produce diseases due to cytolytic infections. We have isolated a herpesvirus from a bovine vascular endothelial cell culture after continuous subculturing. Typical cytopathic changes were observed in bovine endothelial cell cultures 2 days after inoculation of the virus. The virus had an icosahedral nucleocapsid of 100-150 nm in diameter and an envelope. The sequences of some DNA fragments of the virus were highly homologous to those of the bovine herpesvirus type 4 (BHV-4) strains. The DNA restriction maps of the virus and the reference strains of BHV-4, DN 599 and Movar 33/63 were very similar but not identical. Therefore, the newly isolated virus has been designated Taiwan strain. The presence of BHV-4 DNA in apparently normal bovine endothelial cell cultures was shown by Southern blot hybridization with the BamHI fragment of the newly isolated BHV-4 and was further confirmed by digestion of the DNA with BamHI plus AccI. In conclusion, we have demonstrated that BHV-4 persisted in the bovine endothelial cell cultures and continuous subcultures could lead to the production of infectious viral particles.

Animals↗
PubMed1994

Adaptation of hepatitis C virus for persistent infection in patients with acute hepatitis.

Nucleotide sequencing was used to analyze amino acid substitutions in the putative envelope 1 (E1) and envelope 2/nonstructural 1 (E2/NS1) regions of hepatitis C virus (HCV) to clarify a viral mechanism of persistent infection in three patients with acute hepatitis C who developed chronic hepatitis and two patients with chronic hepatitis. The HCV RNA titer in serum decreased markedly after the onset of acute hepatitis and then re-elevated. During this period, the substitution rate in the E2/NS1 region (especially in the hypervariable region located in the N-terminus) was significantly higher in patients with acute hepatitis than in patients with chronic hepatitis (P < 0.05). When patients with acute hepatitis C became persistent HCV carriers, the substitution rate decreased to the level seen in patients with chronic hepatitis. The amino acid substitution rate in the E1 region in the acute phase was similar to that found in the chronic HCV carrier state. These observations suggest that rapid substitution of the amino acid sequence in the hypervariable region of the E2/NS1 region may be one of the mechanisms of persistent HCV infection.

Acute Disease↗