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PubMed1979

[Nature and significance of persistent infections (author's transl)].

The "persistent" viral infections, besides "subclinical" infections, pertain to the vast group of "clinically inapparent" infections. They differ from subclinical infections by a temporally unlimited "co-existence" with the pathogen. Pathogenetically, three forms of development are possible: 1. latent infections, 2. tolerated infections, 3. occult infections. Persistent viral infections are the inexhaustible reservoir for many viruses. To the organism affected they may be of benefit (infection immunity, interference, paraimmunity) or of disadvantage (activation of the infection with conversion into a disease, cause of many chronic, slowly developing disease processes, immunopathogenic consequences), the disadvantages prevailing. To the environment, persistent infections are invisible sources of danger as they produce carriers and chronic carriers.

Carrier State↗
PubMed2004

Bovine herpesvirus 4 infects differentiated neuronal cells in culture and establish persistent infection upon selection.

Bovine herpesvirus 4 (BoHV-4) is a gammaherpesvirus with no clear disease association. Although BoHV-4 is not considered a neurotropic virus, it has been detected in peripheral and/or central nervous system tissues during persistent infection (Lopez et al, 1996, Microb Pathogen 21: 47-58; Yamamoto et al, 2000, Arch Virol 145: 2363-2370; Asano et al, 2003, J Vet Med Sci 65: 87-93). However, the direct interaction between BoHV-4 and neurons has not been studied so far. The authors investigated the interaction of BoHV-4 with N2a (neuroblastoma cell line) cells through the use of two recombinant viruses (BoHV-4/26A3 neo and BoHV-4EGFP?TK). Because of the unique biological characteristics of N2a cells, which differentiate in neuron-like cells producing dendrites, axon, and specific neuronal markers, the authors found that BoHV-4 infects differentiated N2a cells and a persistent infection can be established. BoHV-4 persistently infected N2a cells produce infectious viral particles, which do not interfere with cellular differentiation.

Animals↗
PubMed1990

Characterization of human parainfluenza virus type 3 persistent infection in cell culture.

Three cell lines persistently infected with human parainfluenza virus type 3 were characterized on a molecular level in this study. All six structural protein genes were transcribed into monocistronic RNAs in the persistently infected cells. In both acutely and persistently infected cells, polycistronic transcripts were abundant, although the ratio of polycistronic to monocistronic transcripts was reduced in the persistently infected cells. Each of the persistently infected cell lines contained a distinct subgenomic RNA species. The subgenomic RNAs were present in purified nucleocapsid cores, indicating that they represent viral genome RNA, were far more abundant than full-length RNA, and were stably maintained through at least 36 cell passages. Nucleotide sequence analysis of the subgenomic RNAs from two of the persistently infected cell lines revealed that the 5' ends are identical to that of the standard genome. Hybridization experiments with oligonucleotide probes showed that both fragments retain sequences from the 5' end of the standard genome and contain approximately 1,200 nucleotides (cell line 1) and 1,500 nucleotides (cell line 2) of the polymerase gene sequence. The demonstration of several alterations in viral gene expression in persistently infected cells offers insight into the factors associated with persistence of parainfluenza virus 3.

Animals↗
PubMedDate not supplied

[Persistent infection in murine L cells infected with the parainfluenza virus SV5].

Persistent infection of mouse L cells was achieved by serial passages of undiluted parainfluenza SV5 virus. At the level of the 10--12th passage a stationary noncytocidal type of persistent infection was established. A low level of the infectious virus produced by the persistently infected cells was observed; the number of cells synthesizing the virus-specific antigen detectable by immunofluorescence was high. Persistently infected cells were resistant to the infection with the homologous virus and sensitive to superinfection with heterologous viruses. The persisting virus had marked interfering activity. The possibility of participation of defective interfering particles and endogenous oncornavirus in the maintenance of the persistent infection is discussed.

Animals↗
PubMed2007

Peptidomic analysis of human peripheral monocytes persistently infected by Chlamydia trachomatis.

Peptidomic analysis using Differential Peptide Display (DPD) of human peripheral blood mononuclear cells (PBMC) mock-infected or persistently infected by Chlamydia trachomatis (CT) revealed 10 peptides, expressed upon CT infection. Analysis of these 10 candidates by tandem mass spectrometry enabled the determination of seven candidates as fragments from the precursors (I) ferritin heavy chain subunit, (II) HLA class II histocompatibility antigen, (III) vimentin, (IV) indoleamine 2,3-dioxygenase, (V and VI) pre-B cell enhancing factor (PBEF), and (VII) Interleukin-8 (CXCL8). The identified candidates proved the presence of anti-bacterial and immunologically active monocytic proteins after CT infection.

Chlamydia trachomatis↗
PubMed1991

Changes in cell gene expression in human leukemic cells persistently infected with vaccinia virus.

Persistent viral infections in vitro are useful systems to study the coevolution of virus and cell populations. Persistent infection of mouse Friend erythroleukemic cells (FEL) with vaccinia virus results in profound changes of the virus as well as of the cells. To investigate phenotypic changes of other cell types, we have established a persistent infection with vaccinia virus in a human leukemic cell line (K562). This cell line can be induced to differentiate along the erythroid pathway synthesizing embryonic and fetal globins, thus providing a system in which specific genes can be stimulated. After serial passage, the persistently infected cells (K562vac) became spontaneously differentiated, as shown by the increase in the number of cells producing hemoglobin (benzidine positive cells), and resistant to superinfection. These phenotypic changes of the cells were not accompanied by changes in the viral population. Hybridization of cellular RNA with cloned embryonic and fetal globin genes indicated that uninduced K562 cells do not express these genes, whereas cells induced by hemin or butyrate express G gamma (fetal globin) epsilon and zeta (embryonic globins) genes. By contrast vaccinia infected cells spontaneously express the G gamma gene. These results demonstrate that persistent infection with vaccinia virus elicited phenotypic changes in the infected cell population; in this case the constitutive expression of fetal hemoglobin.

Cell Line↗
PubMed1979

Infective substructures of measles virus from acutely and persistently infected cells.

Ribonucleoprotein from cells acutely or persistently infected with measles virus were shown to be infectious by the calcium phosphate technique. Very little or no infectivity was obtained when calcium phosphate precipitation was omitted. Electron microscopy showed that the majority of ribonucleoprotein structures isolated from acutely infected cells were folded, whereas those from persistently infected cells were linear in appearance.

Animals↗
PubMed1978

Cytomegalovirus infection in guinea pigs. I. Viremia during acute primary and chronic persistent infection.

Studies on the pathogenesis of cytomegalovirus (CMV) infection in guinea pigs have revealed two distinct phases of infection, without any signs of clinical disease. During acute primary infection, viremia was easily demonstrated and infectious virus was recovered from various tissues, including lung, spleen, and kidney, of the infected animal two to 10 days after inoculation. Chronic persistent infection was readily established thereafter. In animals with chronic persistent infection with high levels of circulating antibody, infectious virus was consistently isolated from the salivary gland and pancreas. Evidence of CMV in the blood of the persistently infected animals was detected only occasionally and only when a highly sensitive method and/or a large inoculum was used. However, the anticoagulant heparin was found to inactivate CMV significantly during collection of blood. These data suggest that CMV was indeed circulating in the blood of apparently health but persistently infected animals for prolonged periods. Such infected blood could conceivably be the source of CMV infection when large quantities of blood are given to susceptible recipients.

Acute Disease↗
PubMed1984

Establishment and maintenance of persistent infection by the Phlebovirus Toscana in Vero cells.

Persistent infections were established by serial undiluted passages of the Toscana virus of the genus Phlebovirus in Vero cells. Persistence was maintained through more than 70 passages over a period of 2 years. The persistently infected cells were morphologically similar to the parental Vero cells and released variable amounts of infectious virus. A small percentage of the persistently infected cells produced infectious virus while a larger percentage was shown to possess viral antigens by fluorescent antibody staining. Temperature sensitivity and host cell interferon production were not involved in establishment or maintenance of persistence. The persistently infected cultures were resistant to superinfection with homologous Toscana virus, but they were susceptible to superinfection with heterologous viruses of different genera or families. Toscana virus persistently infected cells showed a selective graded resistance to the replication of other Phleboviruses. Additionally, the virus from persistently infected cells interfered with the replication of standard Toscana virus when they co-infected normal cells. The characteristics of the persistently infected cultures are compatible with some of the characteristics described for the persistence mediated by defective-interfering particles of other viruses.

Animals↗
PubMed1982

Characterization of a hamster brain cell line persistently infected with measles virus.

A persistent infection of measles virus in hamster brain cell cultures was established. Hamster brain cells were transformed with a human papovavirus strain BK and infected with a wild-type measles virus in order to get the cell line persistently infected with measles virus. About 75 per cent of these M-HB/MVB-cells were measles virus-infected. The cells released only small amount of infectious virus and produced low levels of interferon-like activity into the growth medium. During the first 50 passages no large syncytia typical of a lytic measles virus infection were seen. The products of measles virus infection in the cells and in cell culture fluids were followed at two temperatures. Another cell line persistently infected with measles virus (Lu-carrier-cells, 28) was investigated in parallel. In both cell lines measles antigens were cytoplasmic, but during the observation period large amounts of measles nucleocapsid accumulated in the nuclei of the M-HB/MVB-cells. The virus-specific protein synthesis in M-HB/MVB-cells was weak and the intracellular amount of immunoreactive measles nucleocapsid was only 50 per cent (600 ng/10(5) infected cells) of the (1200 ng/10(5) cells) found in Lu-carrier-cells. Also the release of nucleocapsid was minimal in hamster brain cells. The decreased temperature had no clear-cut effect on virus-specific protein synthesis or on the release of the virus-specific products.

Animals↗
PubMed2006

Continuous recruitment of naive T cells contributes to heterogeneity of antiviral CD8 T cells during persistent infection.

Numerous microbes establish persistent infections, accompanied by antigen-specific CD8 T cell activation. Pathogen-specific T cells in chronically infected hosts are often phenotypically and functionally variable, as well as distinct from T cells responding to nonpersistent infections; this phenotypic heterogeneity has been attributed to an ongoing reencounter with antigen. Paradoxically, maintenance of memory CD8 T cells to acutely resolved infections is antigen independent, whereas there is a dependence on antigen for T cell survival in chronically infected hosts. Using two chronic viral infections, we demonstrate that new naive antigen-specific CD8 T cells are primed after the acute phase of infection. These newly recruited T cells are phenotypically distinct from those primed earlier. Long-lived antiviral CD8 T cells are defective in self-renewal, and lack of thymic output results in the decline of virus-specific CD8 T cells, indicating that newly generated T cells preserve antiviral CD8 T cell populations during chronic infection. These findings reveal a novel role for antigen in maintaining virus-specific CD8 T cells during persistent infection and provide insight toward understanding T cell differentiation in chronic infection.

Animals↗
PubMed1983

Defective viral RNAs in Aedes albopictus C6/36 cells persistently infected with Semliki Forest virus.

A persistent infection of Semliki Forest virus (SFV) has been established in Aedes albopictus C6/36 cells. Only a small number of cells survived the initial infection with this RNA virus and gave rise to a persistently infected culture which produced continuously small amounts of infectious virus. To investigate whether defective viral RNA was analyzed early and late after infection by blot hybridizations. Several defective viral RNAs were detected with a common sequence corresponding to the 3' end of the viral genome during and after the establishment of the persistent infection. These defective viral RNAs resemble the defective interfering RNAs in vertebrate cells generated during serial undiluted passages of standard SFV. The defective viral RNAs are rarely released from cells as virions. The rapid generation of defective viral RNAs may be important for the establishment of a persistent infection in mosquito cells.

Aedes↗
PubMed1979

Temperature sensitivity of the arenavirus junin isolated from persistently infected Vero cells.

A persistently infected cell culture was established from Vero cells surviving primary infection with wild-type Junin virus (JVwt). The cells were refractory to superinfection by both Junin virus and the related Tacaribe virus. Replication of virus released from the persistently infected cells (JVpi) was inhibited at 39 degrees. JVpi did not interfere with JVwt at 37 degrees, and it was inactivated at 37, 40, 43, 46 and 50 degrees much more rapidly than was JVwt.

Arenaviridae↗
PubMed2006

Challenge with Bovine viral diarrhea virus by exposure to persistently infected calves: protection by vaccination and negative results of antigen testing in nonvaccinated acutely infected calves.

Calves persistently infected (PI) with Bovine viral diarrhea virus (BVDV) represent an important source of infection for susceptible cattle. We evaluated vaccine efficacy using calves PI with noncytopathic BVDV2a for the challenge and compared tests to detect BVDV in acutely or transiently infected calves versus PI calves. Vaccination with 2 doses of modified live virus vaccine containing BVDV1a and BVDV2a protected the calves exposed to the PI calves: neither viremia nor nasal shedding occurred. An immunohistochemistry test on formalin-fixed ear notches and an antigen-capture enzyme-linked immunosorbent assay on fresh notches in phosphate-buffered saline did not detect BVDV antigen in any of the acutely or transiently infected calves, whereas both tests had positive results in all the PI calves.

Animals↗
PubMed1988

Establishment and characterization of St Louis encephalitis virus persistent infections in Aedes and Culex mosquito cell lines.

Persistent infections with St Louis encephalitis (SLE) virus were established in three mosquito cell lines (Aedes albopictus, A. dorsalis and Culex tarsalis) and were maintained for over 2 years. All three persistently infected cell cultures shared two features: (i) no overt cytopathic effect and (ii) a relatively high proportion of cells infected (41 to 85%). The Aedes persistently infected cultures were resistant to superinfection with the homologous virus but not heterologous viruses. Two significant differences were observed between the Aedes and C. tarsalis persistently infected cell cultures: (i) viral titres in the A. albopictus and A. dorsalis cell cultures decreased slowly over time (the decrease was particularly marked in the A. albopictus cell cultures), whereas titres in the C. tarsalis cell cultures remained relatively constant and (ii) the addition of anti-SLE virus antibody led to decreased virus production in the C. tarsalis cell cultures (one of two cultures was cured of infection), whereas antibody had no effect on the persistently infected Aedes cell cultures. These results suggest that there may be significant differences in the regulation of viral replication and the maintenance of flavivirus persistent infections in mosquito cell lines of different origins.

Aedes↗