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PubMed1988

Phenotypes of St Louis encephalitis virus mutants produced in persistently infected mosquito cell cultures.

Viral mutants that appeared during long-term persistent infections of mosquito cell cultures (Aedes albopictus, A. dorsalis and Culex tarsalis) with St Louis encephalitis virus were characterized. Evidence was obtained for the presence of temperature-sensitive mutants in the A. dorsalis and C. tarsalis persistently infected cultures, and small plaque mutants were predominant in all cultures except one of two cell cultures of C. tarsalis. Virus from persistently infected A. albopictus cell cultures was growth-restricted in Vero and C. tarsalis cells. One of two persistently infected A. dorsalis cell cultures also produced viral mutants that were growth-restricted in C. tarsalis cells. Further, Western blots of persistently infected A. albopictus cell extracts showed an overproduction of capsid (C) and envelope (E) structural proteins and reduced production of an Mr 27K protein (p27) which was immunologically related to the E protein. In contrast, the production of E and C proteins in persistently infected C. tarsalis cultures was consistent with the amount of infectious virus present, whereas p27 was relatively overproduced. These observations suggest that the host cell has an important influence on both the types and relative quantities of viral mutants that accumulate during long-term persistent infections.

Aedes↗
PubMed2006

The cytokine balance in the maintenance of a persistent infection with Salmonella enterica serovar Typhimurium in mice.

ClpXP, serine protease-disrupted mutant of Salmonella enterica serovar Typhimurium chi3306 exhibits attenuated but persistent infection in mice. During infection with S. enterica serovar Typhimurium ClpXP-disrupted mutant, gamma interferon (IFN-gamma) produced by CD4+ cells was up-regulated on day 10 and tumor necrosis factor-alpha (TNF-alpha) produced by CD8+ cells was up-regulated on day 30 after infection. Treatment of monoclonal antibodies against cytokines showed that IFN-gamma and interleukin 10 (IL-10) were involved in maintenance of growth of S. Typhimurium mutant on day 10 after infection, and IFN-gamma, TNF-alpha and transforming growth factor-beta (TGF-beta) were involved in maintenance of growth of this bacterium on day 30 after infection. During persistent infection of S. Typhimurium mutant, IFN-gamma, TNF-alpha, IL-10 and TGF-beta may play different roles to maintain the persistent infection. The cytokine balance might be important in persistent infection with ClpXP-disrupted S. enterica serovar Typhimurium.

Animals↗
PubMed1979

Evolution of multiple genome mutations during long-term persistent infection by vesicular stomatitis virus.

Persistent infection of BHK21 cells was established with cloned vesicular somatitis virus plus purified Dl particles and maintained in vitro for over 5 years. After 1 year of persistence, the infectious virus RNA genome had evolved several oligonucleotide map changes, and numerous changes had accumulated by 3.5 years. Additional evolution occurred by the fourth year and continued until the fifth year. In contrast, repeated passage of virus in acute infections of several cell types in vitro or in vivo did not lead to detectable oligonucleotide map changes. The short Dl particle originally used to co-infect with infectious virus in establishing persistent infection has been displaced by an ever present and constantly changing population of other Dl particles of differing sizes and radically differing oligonucleotide maps. We conclude that the genomes of both infectious VSV and its Dl particles undergo continuous evolutionary change during years of persistence. In the infectious virus, these changes involve hundreds of mutations which are usually expressed as poorly replicating, temperature-sensitive, small plaque mutants. These are stable mutants which do not revert to wild-type when passaged repeatedly in acute infections at 37 or 33 degrees C. It appears that the sequestered intracellular environment of persistently infected cells favors rapid and continuous virus evolution.

Animals↗
PubMed1995

Serum concentrations of thyroid hormones in calves with a transient or persistent infection with bovine viral diarrhoea virus.

Calves persistently infected with bovine viral diarrhoea virus (BVDV) often appear small for their age and it is possible that the virus interferes with their body metabolism by affecting the production of hormones. In this study, the serum concentrations of thyroxine (T4) and triiodothyronine (T3) were measured in calves with transient or persistent BVDV infections. The mean (SD) concentrations of T3 and T4 were lower (P < 0.001) in the persistently infected calves (1.79 [0.67] and 69.2 [23.8] nmol litre-1, respectively) from three dairy herds than in age-matched control calves (2.39 [0.72] and 93.4 [22.1] nmol litre-1, respectively). In each herd, the thyroid hormone levels were also lower in the persistently infected calves than in the controls, the differences being significant (P < 0.05) with the exception of the T3 level in one herd. The girth of the infected calves over the heart was less (P < 0.001) than that of the controls, and, among the infected calves but not among the controls, there was a significant correlation between heart girth and the levels of T3 (r = 0.72, P < 0.001) and T4 (r = 0.60, P < 0.01). Six calves not previously exposed to BVDV were infected through nose-to-nose contact with a persistently infected calf. Their T3 and T4 levels were decreased seven days (P < 0.05 and not significant, respectively) and nine days (P < 0.001 and P < 0.01, respectively) after the infection, when the clinical signs of the disease appeared.

Animals↗
PubMed1993

Persistent infection with human parainfluenza virus 3 in CV-1 cells: analysis of the role of defective interfering particles.

Persistent infection of cultured cells with human parainfluenza virus type 3 (HPF3), established following infection at high multiplicity, has been associated with the presence of one or more viral defective-interfering (DI) particles in addition to standard viral genomes. We recently showed that persistent infection can also be established after low multiplicity infection, a condition not generally associated with amplification of DI particles. The association of DI particle genomes with persistent infection was therefore studied after infection with low multiplicity. Persistently infected cell cultures were established after low multiplicity infection with HPF3 in the presence of exogenous bacterial neuraminidase, and viral nucleocapsid RNA was analyzed for the presence of DI genomes at each passage after infection. In addition, the timing of DI particle appearance was assessed after infection with high multiplicity, a condition known to favor the amplification of DI particles. DI particles genomes did not appear until at least seven passages of persistently infected cell cultures, after either low or high multiplicity infection. Our data suggest that DI particles are not required for establishment of persistent infection of CV-1 cells by HPF3 and that DI particles are not generated early in infection. Despite reports of the association of paramyxovirus DI particles with persistent infection in culture, the role of these particles in HPF3 persistence is unknown; our findings offer insight into the complex interplay of viral and host factors in persistent infection.

Blotting, Northern↗
PubMed1993

Identification of a region of the poliovirus genome involved in persistent infection of HEp-2 cells.

Poliovirus mutants were selected during the persistent infection of human neuroblastoma cells. These viruses could establish secondary persistent infections in HEp-2 nonneural cells. We report the identification of a region of the genome of a persistent virus (S11) that was sufficient to confer to a recombinant virus the phenotype that causes persistent infection in HEp-2 cells. This region, between nucleotides 1148 and 3481, contained 11 missense mutations mapping exclusively in the genes of capsid proteins VP1 and VP2. Because recombinant viruses carrying only one of these two mutated genes were not able to cause persistent infection, it seems very probable that two or more mutations in these genes are required for expression of the phenotype that causes persistent infection.

Capsid↗
PubMed1986

Vero cells persistently infected with Tacaribe virus: role of interfering particles in the establishment of the infection.

Eight Vero cell sublines (Vero T) persistently infected with wild type Tacaribe virus replicated in different hosts were established. In order to unravel the mechanism involved in the initiation and maintenance of persistence, the properties of virus shed by the sublines and the presence of interfering particles (IP) were analyzed. During the course of infection, persistent virus (Tac-pi) underwent mutations although no consistent pattern of virus evolution was observed. ts mutants were isolated from two Vero T sublines, whereas a slow growth variant was shed by another. The remaining sublines released virus resembling wt parental virus. Except for Vero T1 sublines, Vero T cultures shed no detectable IP. These results emphasize the point that neither the emergence of virus mutants nor the synthesis of IP is essential for the maintenance of the persistent state. To define the role of IP in the initiation of persistence, coinfection experiments with a characterized inoculum were performed. For that purpose, attempts were made to obtain IP stocks free from pfu by serial transfers of undiluted virus. Neither enrichment nor amplification of IP occurred, and virus stocks were freed of infectious virus by UV irradiation. If normal Vero cells were infected with Tac-pi virus released by Vero T2, Vero T3, Vero T4, Vero T5, Vero T6, Vero T7 and Vero T10 sublines, a complete destruction of the monolayer without cell recovery was observed. In contrast, parental and Vero T1 viruses always originated persistently infected sublines. Similarly, the addition of IP to virus inocula constituted by Tac-pi viruses released by Vero T2, Vero T3, Vero T4, Vero T5, Vero T6, Vero T7 and Vero T10 sublines gave rise to persistently infected cultures. These results suggest that although IP are not important by themselves in the maintenance of persistence, they play a major role in initiation.

Animals↗
PubMed2001

Study of cattle persistently infected with bovine viral diarrhea virus that lack detectable virus in serum.

OBJECTIVE: To determine whether cattle persistently infected with bovine viral diarrhea virus (BVDV) that lack virus detectable in serum by use of the immunoperoxidase microtiter assay (IPMA) can transmit the virus to susceptible herdmates and determine prevalence of these cattle. DESIGN: Clinical trial and serologic survey. SAMPLE POPULATION: 2 cattle and 1,952 blood samples. PROCEDURE: A persistently infected cow in which virus could not be detected in serum was housed with a BVDV-seronegative steer. Blood and nasal swab specimens were tested via virus isolation and serum virus neutralization. Parallel WBC preparations and sera from blood samples of 1,952 adult cows were screened for BVDV by use of IPMA. RESULTS: The steer seroconverted to BVDV within 4 weeks of contact with the cow. Virus was detected in sera and WBC of 5 adult cows that were verified as persistently infected by retest 3 weeks later. Cattle persistently infected with BVDV in which virus could not be detected in both serum and WBC by use of IPMA were not found. CONCLUSION AND CLINICAL RELEVANCE: Cattle persistently infected with BVDV in which virus cannot be detected in serum by use of IPMA may serve as virus reservoirs for infecting susceptible cattle. Persistent infection was detected at a prevalence of 0.26%. Screening adult cattle by use of IPMA on serum samples appears to be a reliable means of detecting persistent infection with BVDV. Prevalence of cattle persistently infected with BVDV that have negative results of IPMA on serum is extremely low.

Animals↗
PubMed1988

Varicella-zoster virus DNA from persistently infected cells contains novel tandem duplications.

A persistent infection with varicella-zoster virus was established in the Mewo human melanoma cell line. This persistently infected cell line went through periodic crises of virus-induced cell killing and then recovery. Analyses of viral DNA derived from the persistently infected cultures revealed that novel viral nucleic acid rearrangements had been generated. These viral DNA sequences were derived from a specific region of the inverted repeat sequence of the genome flanking the short unique genome segment. The novel DNA was of various lengths, each generated by tandem duplication of an approximately 2760 base pair sub-sequence of the normal viral inverted repeat. These novel sequences were inserted into an otherwise apparently normal genome.

Antigens, Viral↗
PubMed1988

Oligo-2',5'-adenylate synthetase activity in K562 cell lines persistently infected with measles or mumps virus.

Fluctuation of oligo-2',5'-adenylate synthetase (2-5AS) activity was examined in K562 cells infected with vaccine strains of measles virus (strains AIK-C and CAM-70) and mumps virus (strains Torii and Miyahara). Persistent infection was easily established in the mumps virus-infected cells without significant cytolysis or cell killing. In contrast, most of the cells infected with measles virus were killed by extensive cytolysis within 3 to 4 days. The small number of cells that did survive became persistently infected. That these persistently infected cells carried a virus antigen was confirmed by fluorescein isothiocyanate-labelled anti-measles virus rabbit antiserum and anti-mumps virus rabbit antiserum. The cells produced infectious progeny virus as well as interferon (IFN). Little induction of 2-5AS activity by IFN was demonstrated during the early stages of infection by these viruses. Similar results were observed in some of the persistently infected cells but not, however, K-CMP cells (K562 cells persistently infected with CAM-70) or K-MMP cells (K562 cells persistently infected with Miyahara). Failure to induce 2-5AS activity was unchanged in cells cultured for more than 6 months. The decrease of 2-5AS activity observed in K-MTP cells (K562 cells persistently infected with Torii) was the result of suppression of transcription of 2-5AS mRNA. On the other hand, a normal level of mRNA was found in K-AKP cells (K562 cells persistently infected with AIK-C). Therefore, it is suggested that the decrease of 2-5AS activity in K-AKP cells may be due to a failure to translate 2-5AS mRNA.

2',5'-Oligoadenylate Synthetase↗
PubMed1997

Performance, survival, necropsy, and virological findings from calves persistently infected with the bovine viral diarrhea virus originating from a single Saskatchewan beef herd.

Fifty-one calves from 652 cows and heifers that calved on a Saskatchewan ranch in 1992 were identified as persistently infected with bovine viral diarrhea virus (BVDV), based on virological and necropsy findings. Herd records suggested a further 20 calves that died between birth and weaning were probably also persistently infected. Subsequent to weaning, all surviving persistently infected calves were transferred to one pen in a 10,000 head commercial feedlot, to mimic normal management practice in western Canadian beef herds. On average, when compared with healthy, BVDV-negative herdmates, persistently infected calves were "poor doers" and had poor survivability, with only 4 persistently infected calves surviving to 1 year of age. There was no difference (P > 0.05) in survival between male and female persistently infected calves. The clinical, pathological, and virological findings from these persistently infected calves varied over time. The majority of persistently infected calves had gross pathological lesions at necropsy, consistent with mucosal disease. However, approximately 25% of the persistently infected calves had gross pneumonic lesions at necropsy, with no or only mild lesions of mucosal disease. A wide variety of other lesions were also noted in persistently infected calves at necropsy. Therefore, the possibility that BVDV-induced lesions can be misdiagnosed is very real. The results of this study indicate that persistent infection with BVDV should always be considered in calves with chronic ill thrift, chronic enteritis, or respiratory disease.

Animals↗
PubMed1995

Persistent infection of cultured cells with mouse hepatitis virus (MHV) results from the epigenetic expression of the MHV receptor.

The A59 strain of murine coronavirus mouse hepatitis virus (MHV) can cause persistent infection of 17C1-1 cells and other murine cell lines. Persistently infected cultures released large amounts of virus (10(7) to 10(8) PFU/ml) and were resistant to superinfection with MHV but not to infection with unrelated Semliki Forest and vesicular stomatitis viruses. The culture medium from persistently infected cultures did not contain a soluble inhibitor such as interferon that protected uninfected cells from infection by MHV or vesicular stomatitis virus. The persistent infection was cured if fewer than 100 cells were transferred during subculturing, and such cured cultures were susceptible to reinfection and the reestablishment of persistent infection. Cultures of 17C1-1 cells that had been newly cloned from single cells consisted of a mixture of MHV-resistant and -susceptible cells. 17C1-1/#97 cells, which were cured by subcloning after 97 passages of a persistently infected culture over a 1-year period, contained 5 to 10% of their population as susceptible cells, while 17C1-1/#402 cells, which were cured by subcloning after 402 passages over a 3-year period, had less than 1% susceptible cells. Susceptibility to infection correlated with the expression of MHV receptor glycoprotein (MHVR [Bgp1a]). Fluorescence-activated cell sorter analysis with antibody to MHVR showed that 17C1-1/#97 cells contained a small fraction of MHVR-expressing cells. These MHVR-expressing cells were selectively eliminated within 24 h after challenge with MHV-A59, and pretreatment of 17C1-1/#97 cells with monoclonal antibody CC1, which binds to the N-terminal domain of MHVR, blocked infection. We conclude that the subpopulation of MHVR-expressing cells were infected and killed in acutely or persistently infected cultures, while the subpopulation of MHVR-nonexpressing cells survived and proliferated. The subpopulation of MHVR-negative cells produced a small proportion of progeny cells that expressed MHVR and became infected, thereby maintaining the persistent infection as a steady-state carrier culture. Thus, in 17C1-1 cell cultures, the unstable or epigenetic expression of MHVR permitted the establishment of a persistent, chronic infection.

3T3 Cells↗
PubMed1983

Viral proteins and RNAs in BHK cells persistently infected by lymphocytic choriomeningitis virus.

Some Syrian hamster cell lines persistently infected with lymphocytic choriomeningitis virus (LCMV) do not produce extracellular virus particles but do contain intracytoplasmic infectious material. The proteins of these cells were labeled with [35S]methionine or with [3H]glucosamine and [3H]mannose, and immunoprecipitates were prepared with anti-LCMV sera. A substantial amount of the LCMV nucleocapsid protein (molecular weight about 58,000) was detected, along with GP-C, the precursor of the virion glycoproteins GP-1 and GP-2. GP-1 and GP-2 themselves were not detected. A new method of transferring proteins electrophoretically from sodium dodecyl sulfate-polyacrylamide gels to diazotized paper in high yield revealed several additional LCMV proteins present specifically in the persistently infected cells, at apparent molecular weights (X10(3] of 112, 107, 103, 89, 71 (probably GP-C), 58 (nucleocapsid protein), 42 to 47 (probably GP-1), and 40 (possibly GP-2). By iodinating intact cells with I3, GP-1 but not GP-2 or GP-C was revealed on the surfaces of the persistently infected cells, whereas both GP-1 and GP-C were found on the surfaces of acutely infected cells. The absence of GP-C from the plasma membrane of the persistently infected cells might be related to defective maturation of the virus in these cells. Cytoplasmic viral nucleoprotein complexes were labeled with [3H]uridine in the presence or absence of actinomycin D, purified partially by sedimentation in D2O-sucrose gradients, and adsorbed to fixed Staphylococus aureus cells in the presence of anti-LCMV immunoglobulin G. Several discrete species of viral RNA were released from the immune complexes with sodium dodecyl sulfate. Some were appreciably smaller than the 31S and 23S species of standard LCMV virions, indicating that defective interfering viral RNAs are probably present in the persistently infected cells. Ribosomal 28S and 18S RNAs, labeled only in the absence of actinomycin D, were coprecipitated with anti-LCMV serum but not with control serum, indicating their association with LCMV nucleoproteins in the cells.

Animals↗
PubMed2004

Markedly reduced severity of Dengue virus infection in mosquito cell cultures persistently infected with Aedes albopictus densovirus (AalDNV).

AalDNV-infected C6/36 cells serially passaged for over 10 weeks showed a decline in percentage of anti-AalDNV-positive cells (APC) from an initial 92% to approximately 20%. Cultures of persistent APC were indistinguishable from uninfected cultures by direct microscopy but most stained cells from early APC passages had enlarged nuclei with eosinophilic inclusions, while late APC passages had few and naive cells none. Super challenge of persistent APC cultures did not increase percentage APC and supernatants from persistent APC cultures gave low APC (40%) in naive C6/36 cell cultures. When challenged with dengue virus serotype 2 (DEN-2), naive C6/36 cells showed severe cytopathic effects (CPE) and high mortality within 4 days, as did early passage APC cultures. Remarkably, DEN-2 infections in persistent APC cultures were much less severe, being characterized by reduced DEN-2 infection percentage, retarded DEN-2 virion production, no CPE and no significant mortality. Reasons for rapid reduction in APC and resistance to superinfection upon serial passage remain unproven but may relate to production of AalDNV-defective interfering particles (DIP) by molecular mechanisms still open to speculation. More difficult to explain is cross-protection against DEN-2-induced mortality seen in persistent APC cultures. However, by comparison to work on shrimp viruses, we speculate that this may involve blockage of viral-triggered apoptosis. The phenomena described raise questions regarding the potential for persistent infections by unknown viruses to confound experimental results with insect cell lines.

Aedes↗
PubMed1979

Establishment of persistent infection by parainfluenza virus type 3: role of a syncytium inhibitor.

A strain of parainfluenza virus type 3 (para 3) that had undergone a series of undiluted passages failed to produce syncytia when inoculated on to Vero cells at a high m.o.i. The strain repeatedly produced stable persistent infections. Persistently infected cells were resistant to superinfection by homologous virus, showed the presence of virus-specific antigen and shed low quantities of infectious virus into the supernatant fluid. The undiluted passage parainfluenza virus type 3 strain produced a substance that inhibited syncytium formation by homologous virus and by measles virus but appeared to have no effect on virus replication. This inhibitor had no demonstrable effect on unrelated viruses, including some that produced syncytia. It had a mol. wt. between 3500 and 14000, was acid- and heat-labile, and was inactivated by anti-para 3 serum.

Animals↗
PubMed1979

Role of virus variants and cells in maintenance of persistent infection by measles virus.

Hamster embryo fibroblasts persistently infected with a derivative of the Schwarz vaccine strain of measles virus spontaneously released virus particles with an average buoyant density considerably lower than that of the parental virus. The released virus contained all of the measles virus structural proteins and interfered with replication of standard virus. All of the virus structural proteins were associated with a membrane-free cytoplasmic extract from the persistently infected cells. Membrane-free cytoplasmic extracts prepared from Vero cells lytically infected with Schwarz strain measles contained little or no virus envelope structural protein. Maintenance of persistent infection may involve both the presence of virus variants and a defect in the ability of the infected cell to replicate the virus efficiently.

Animals↗
PubMed1998

One amino acid change on the capsid surface of poliovirus sabin 1 allows the establishment of persistent infections in HEp-2c cell cultures.

Poliovirus mutants (PVpi) selected during the persistent infection of human neuroblastoma cells can establish secondary persistent infections in nonneural HEp-2c cells (I. Pelletier, T. Couderc, S. Borzakian, E. Wyckoff, R. Crainic, E. Ehrenfeld, and F. Colbère-Garapin, 1991, Virology, 180, 729-737). Previous results from our laboratory have also shown that, in the genome of PVpi S11 derived from the Sabin 1 strain, the genomic region involved in this phenotype contains 11 missense mutations which map exclusively to the genes encoding the capsid proteins VP1 and VP2. We report here the identification of precise viral determinants able to confer the capacity to establish persistent infections in HEp-2c cell cultures to the lytic Sabin 1 strain. We used a strategy based on the observation that PVpi, after a few months of persistent infection in HEp-2c cells, tend to regain a more lytic phenotype in uninfected HEp-2c cell cultures. We constructed mutant viruses carrying only a few mutations potentially involved in the phenotype of persistence. Two mutations were identified, one corresponding to the substitution His>Tyr of amino acid 142 of VP2 and another corresponding to the substitution Val>Ile of amino acid 160 of VP1. Mutants carrying one or the other of the two determinants established persistent infections in HEp-2c cell cultures in about 20% of the infections. Higher frequencies were obtained with the mutant carrying both determinants (30%), and with PVpi S11 (63%), indicating that the effects of several determinants can be cumulative. The two determinants are localized on the capsid surface in a region known to be involved in the interactions between poliovirus and its cell receptor and in fact, we demonstrate here that in the case of the two persistent mutants, these interactions are modified.

Amino Acid Substitution↗
PubMed2005

Molecular characterization of Jurkat cells persistently infected with vaccinia virus mutant vp811.

Previous reports from this laboratory demonstrated that persistent infections could be established in Jurkat cells with wild-type vaccinia virus (Jvac). The infected cells elicit increased expression of IL-2, IL-2Ralpha and IL-6 but not of IL-1beta nor of interferon-gamma. The persistently infected cells are also capable to transactivate the LTR gene of HIV-1 virus (HIV-1LTR). In addition, NFkappabeta and NFAT are found activated in Jvac. To find out whether the gene(s) responsible for establishment, maintenance and molecular characteristics of persistently infected cells are located in the terminal ends of the molecule, Jurkat cells were infected with a deletion mutant Vp811 that lacks 32.7 and 14.9 kb at the left and right terminal, respectively. The results indicate that the deletion mutant is capable of establishing persistent infections. The persistently infected cells show a similar pattern of expression to that observed in Jvac cells. It is concluded that the viral gene(s) involved in persistence and molecular cellular changes is (are) present in the mutant.

DNA, Viral↗