Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “VIRUSES”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 109 records · Page 6Linked to original sources
PubMed1995

Human immunodeficiency virus infection as risk factor for mother-to-child hepatitis C virus transmission; persistence of anti-hepatitis C virus in children is associated with the mother's anti-hepatitis C virus immunoblotting pattern.

To determine the rate of vertical transmission of hepatitis C virus (HCV), we prospectively studied 45 babies born to anti-HCV-positive women with or without concomitant infection with the human immunodeficiency virus (HIV). We performed a second-generation recombinant immunoblotting assay, alanine transaminase (ALT) evaluation, and HCV-RNA testing on sera from 27 infants of HCV+, HIV- mothers and 18 babies of HCV+, HIV+ women, at birth and thereafter. After birth, HCV antibodies progressively disappeared within 12 months in all children but one, whose mother was HCV+, HIV+; this child was the only one who showed detectable levels of HCV-RNA and abnormal ALT values throughout the follow-up (range, 12 to 27 months). Viremia was persistently negative, and ALT levels were continuously normal in the remaining infants, showing that "seronegative" infection with HCV was absent in both groups. Clearance of passively acquired anti-HCV antibodies was found to be slower among babies born to HIV+ mothers (22.3% vs. 3.8% at 12 months, P = .03) and children whose mothers showed three or four anti-HCV reactivities by immunoblotting maintained anti-HCV for longer periods compared with babies born to mothers with one or two anti-HCV reactivities (P = .0001). Seventeen of 27 babies born to HCV+, HIV- mothers were breast-fed, and none of them was infected, confirming the apparent safety for HCV of breast milk. In summary, according to our study, vertical transmission of HCV is an infrequent event, and the presence of HIV in the mother is not an important co-factor for transmission of HCV infection.

Alanine Transaminase↗
PubMed1997

[Herpes viruses--herpes simplex virus, varicella-zoster virus, EB virus, cytomegalovirus].

Herpes simplex encephalitis is the commonest viral encephalitis among individuals, and the mortality has been markedly decreased by the use of vidarabine and acyclovir. Early diagnoses and immediate treatment are essential for favorable prognoses. Neuro-imagings, such as MRI and SPECT, and PCR technique for detection of HSV-DNA in CSF, are useful for early diagnoses, without requiring brain biopsy. Varicella and herpes zoster viruses are complicated, only rarely, with neurological manifestations, such as meningoencephalitis, myelitis, or peripheral neuropathy. Acyclovir is mostly effective in these cases. Neurological complications of Epstein-Barr virus infections are variable, including meningitis, cerebellar ataxia, cranial neuropathy, and Guillain-Barré syndrome. Their prognoses are generally good. Cytomegalovirus encephalitis is one of the common complications in AIDS patients. Its clinical diagnosis is difficult and the prognosis is considered to be poor.

AIDS-Related Opportunistic Infections↗
PubMed1990

Sequential changes in the humoral immune response of pigs to pseudorabies virus after vaccination, exposure to virulent virus, and reactivation of latent virus.

Sequential changes in the humoral immune response of pigs to pseudorabies virus (PRV) after each of several exposures to the virus were evaluated by determining virus neutralization (VN) and radioimmunoprecipitation (RIP) activities of sera collected at selected intervals. Pigs were vaccinated intramuscularly with live attenuated virus (6 pigs), inactivated attenuated virus (6 pigs), or inactivated virulent virus (6 pigs). All pigs were challenged oronasally with virulent virus 3 weeks later and 12 (4 pigs of each vaccine group) were subsequently treated with dexamethasone in an attempt to reactivate latent virus. The relatively low serum titers of VN antibody that were raised by vaccination (titers ranged from 2 to 32) increased markedly (at least 16-fold) for all pigs after exposure to virulent virus. After dexamethasone treatment, the VN titers of 2 pigs increased 16-fold, whereas those of the other 10 dexamethasone-treated pigs and the 6 nontreated pigs either remained the same or increased only minimally (i.e., no more than 2-fold). The results of RIP using 35S-methionine-labeled viral proteins were initially similar to those of VN in that the low levels of serum RIP activity detected after vaccination increased markedly after subsequent exposure to virulent virus. In contrast to VN, however, most pigs (11 of 12) treated with dexamethasone had a clear increase in serum RIP activity. The increase was particularly striking for viral proteins of relatively low (less than 46K) molecular weight. Precipitating activity for 14C-glucosamine-labeled viral glycoproteins was not detected until after pigs were exposed to virulent virus. The increase in RIP activity detected after dexamethasone treatment was likely due to an additional antigenic stimulus associated with virus reactivation. However, virus was isolated from nasal swabs of only 4 of the 12 treated pigs. None of the results appeared to be affected appreciably by the type of vaccine used for initial immunization.

Animals↗
PubMed1975

Murine sarcoma virus related nucleic acid sequences in a non-transforming virus derived from an interspecies pseudotype sarcoma virus.

A number of sarcomagenic viruses recovered from hamster tumors induced originally by Moloney sarcoma virus or several of its mouse pseudotypes appear to be interspecies pseudotypes with structural proteins of hamster type-C viruses and nucleic acid sequences of both mouse and hamster specificity. A non-transforming virus (GLOH-minus) recovered from a sarcomagenic virus preparation obtained from a tumor induced by the Gross pseudotype of Moloney sarcoma virus was previously shown to retain mouse sequences. The ability to discriminate readily between Gross and Moloney viruses by molecular hybridization, especially with regard to thermal stability of inter-strain hybrid molecules, and the stability of Moloney virus sequences in a rat-mouse interspecies pseudotype, made it possible to specify that the mouse virus-specific sequences in GLOH-minus are derived from Moloney virus and not Gross. Thus, even though GLOH-minus is non-transforming in vitro or in vivo, it still retains sequences highly related to Moloney sarcoma virus. The lack of transforming ability is thus probably based on loss or change of specific sequences necessary for transformation at some point in the history of this virus.

AKR murine leukemia virus↗
PubMed1991

Vaccinia virus DNA ligase is nonessential for virus replication: recovery of plasmids from virus-infected cells.

The essentiality of the vaccinia virus DNA ligase gene, SalF 15R, for virus growth was tested by insertional mutagenesis. A plasmid containing E. coli gpt inserted within a large deletion in the DNA ligase gene was transfected into vaccinia virus-infected cells and recombinant viruses selected by three cycles of plaque purification in the presence of mycophenolic acid (MPA). Surprisingly, in some isolates, which replicated in a manner indistinguishable from wild type (WT) virus, the WT gene was replaced by the gpt allele, demonstrating that the DNA ligase gene is nonessential for growth in cultured cells. In other isolates the entire plasmid was integrated into the virus genome by a single crossover event and a functional copy of the DNA ligase was retained. Southern blot analyses of the latter, drug-resistant viruses indicated extra DNA fragments, of sizes inconsistent with predicted viral structures, which represent the plasmid products of homologous recombination. Hirt extracts from cells infected with such multiply plaque purified virus isolates yielded plasmids that produced ampicillin-resistant colonies after transformation of E. coli. These plasmids were of two structures, representing either the original plasmid used for transfection, or a plasmid containing the WT ligase gene rescued by recombination with the virus genome. Similarly, insertional mutagenesis of the vaccinia virus thymidine kinase (TK) gene with gpt yielded plasmids containing mutant or wild type TK alleles when recombinant viruses were selected in MPA. Such plasmids were not isolated when TK minus viruses were selected in 5-bromodeoxyuridine (BUdR).

Animals↗
PubMed1981

Recombinants between temperature-sensitive mutants of rauscher murine leukemia virus and BALB:virus-2: genetic mapping of the Rauscher murine leukemia virus genome.

Recombinant viruses were generated in tissue culture between Rauscher murine leukemia virus (MuLV) temperature-sensitive (ts) mutants restricted at different steps in virus replication and a mouse endogenous xenotropic virus, BALB:virus-2. Mutants used included ts 28, a late mutant which releases noninfectious viruses at 39 degrees C, and ts 29, a double mutant with a ts lesion in its reverse transcriptase and a late block affecting virus budding. Immunological typing of the translational products of clonal recombinant viruses made it possible to establish their partial genetic maps and localize regions of the viral genome affected by different ts lesions. Recombinants involving Rauscher MuLV ts 28 invariably contained BALB-virus-2 p15, p12, and p30 proteins, localizing the late defect in replication by this mutant to the 5' moiety of the viral gag gene. All ts 29-derived recombinants contained the entire BALB:virus-2 gag and pol genes. Substitution of the pol gene is in agreement with the reported thermolability of Rauscher MuLV ts 29 reverse transcriptase (Tronick et al., J. Virol. 16:1476-1482, 1975). Substitution of the gag gene suggests that internal structural proteins are actively involved in the virus budding processing. Rauscher MuLV recombinants were used to establish the genetic map of the Rauscher MuLV genome by T1 oligonucleotide fingerprinting analysis. Detection of Rauscher MuLV T1 oligonucleotides in representative recombinant viruses, whose protein phenotypes were established by immunological techniques, permitted their assignment to specific regions of the viral genome. The genetic map of Rauscher MuLV generated in these studies should be useful for identifying and characterizing the viral gene(s) involved in leukemogenesis.

Animals↗
PubMed2002

Visna virus-induced activation of MAPK is required for virus replication and correlates with virus-induced neuropathology.

It is well accepted that viruses require access to specific intracellular environments in order to proliferate or, minimally, to secure future proliferative potential as latent reservoirs. Hence, identification of essential virus-cell interactions should both refine current models of virus replication and proffer alternative targets for therapeutic intervention. In the present study, we examined the activation states of mitogen-activated protein kinases (MAPKs), ERK-1/2, in primary cells susceptible to visna virus and report that virus infection induces and sustains activation of the ERK/MAPK pathway. Treatment of infected cells with PD98059, a specific inhibitor of the ERK/MAPK pathway, abolishes visna virus replication, as evidenced by extremely low levels of Gag protein expression and reverse transcriptase activity in culture supernatants. In addition, although visna virus-induced activation of MAPK is detectable within 15 min, early events of viral replication (i.e., reverse transcription, integration, and transcription) are largely unaffected by PD98059. Interestingly, further examination demonstrated that treatment with PD98059 results in decreased cytoplasmic expression of gag and env, but not rev, mRNA, highly suggestive of an ERK/MAPK-dependent defect in Rev function. In vivo analysis of ERK-1/2 activation in brains derived from visna virus-infected sheep demonstrates a strong correlation between ERK/MAPK activation and virus-associated encephalitis. Moreover, double-labeling experiments revealed that activation of MAPK occurs not only in cells classically infected by visna virus (i.e., macrophages and microglia), but also in astrocytes, cells not considered to be major targets of visna virus replication, suggesting that activation of the ERK/MAPK pathway may contribute to the virus-induced processes leading to neurodegenerative pathology.

Animals↗
PubMed2003

A virus-virus interaction circumvents the virus receptor requirement for infection by pathogenic retroviruses.

During ongoing C-type retrovirus infection, the probability of leukemia caused by insertional gene activation is markedly increased by the emergence of recombinant retroviruses that repeatedly infect host cells. The murine mink cell focus-inducing (MCF) viruses with this property have acquired characteristic changes in the N-terminal domain of their envelope glycoprotein that specify binding to a different receptor than the parental ecotropic virus. In this report, we show that MCF virus infection occurs through binding to this receptor (termed Syg1) and, remarkably, by a second mechanism that does not utilize the Syg1 receptor. By the latter route, the N-terminal domain of the ecotropic virus glycoprotein expressed on the cell surface in a complex with its receptor activates the fusion mechanism of the MCF virus in trans. The rate of MCF virus spread through a population of permissive human cells was increased by establishment of trans activation, indicating that Syg1 receptor-dependent and -independent pathways function in parallel. Also, trans activation shortened the interval between initial infection and onset of cell-cell fusion associated with repeated infection of the same cell. Our findings indicate that pathogenic retrovirus infection may be initiated by virus binding to cell receptors or to the virus envelope glycoprotein of other viruses expressed on the cell surface. Also, they support a broader principle: that cooperative virus-virus interactions, as well as virus-host interactions, shape the composition and properties of the retrovirus quasispecies.

Animals↗
PubMed1983

Enhanced transformation by a simian virus 40 recombinant virus containing a Harvey murine sarcoma virus long terminal repeat.

We have constructed a recombinant simian virus 40 (SV40) DNA containing a copy of the Harvey murine sarcoma virus long terminal repeat (LTR). This recombinant viral DNA was converted into an infectious SV40 virus particle and subsequently infected into NIH 3T3 cells (either uninfected or previously infected with Moloney leukemia virus). We found that this hybrid virus, SVLTR1, transforms cells with 10 to 20 times the efficiency of SV40 wild type. Southern blot analysis of these transformed cell genomic DNAs revealed that simple integration of the viral DNA within the retrovirus LTR cannot account for the enhanced transformation of the recombinant virus. A restriction fragment derived from the SVLTR-1 virus which contains an intact LTR was readily identified in a majority of the transformed cell DNAs. These results suggest that the LTR fragment which contains the attachment sites and flanking sequences for the proviral DNA duplex may be insufficient by itself to facilitate correct retrovirus integration and that some other functional element of the LTR is responsible for the increased transformation potential of this virus. We have found that a complete copy of the Harvey murine sarcoma virus LTR linked to well-defined structural genes lacking their own promoters (SV40 early region, thymidine kinase, and G418 resistance) can be effectively used to promote marker gene expression. To determine which element of the LTR served to enhance the biological activity of the recombinant virus described above, we deleted DNA sequences essential for promoter activity within the LTR. SV40 virus stocks reconstructed with this mutated copy of the Harvey murine sarcoma virus LTR still transform mouse cells at an enhanced frequency. We speculate that when the LTR is placed more than 1.5 kilobases from the SV40 early promoter, the cis-acting enhancer element within the LTR can increase the ability of the SV40 promoter to effectively operate when integrated in a murine chromosome. These data are discussed in terms of the apparent cell specificity of viral enhancer elements.

Animals↗
PubMed1996

In vivo anti-influenza virus activity of Kampo (Japanese herbal) medicine "Sho-seiryu-to"--effects on aged mice, against subtypes of a viruses and B virus, and therapeutic effect.

When aged BALB/c mice (approximately 6 months old) were treated with a Kampo (Japanese herbal) medicine "Sho-seiryu-to (SST)" (1 g/kg, 10 times) orally from 7 days before to 4 days after the infection and infected with mouse-adapted influenza virus A/PR/8/34 (H1N1 subtype) by nasal site-restricted infection, replication of the virus in the broncho-alveolar cavity was efficiently inhibited at 5 days after infection in comparison with water-treated mice. The antiviral IgA antibody in the broncho-alveolar wash of the SST treated aged mice increased significantly. When mice (7 weeks old) were administered orally with SST (1 and 2 g/kg, 7 times) from 4 days before to 3 days after the infection and infected with mouse-adapted influenza virus A/Guizhou/54/89 (H3N2 subtype) or B/Ibaraki/2/85, replication of the viruses in the nasal cavity and lung were significantly inhibited at 4 days after infection in comparison with control mice. When mice infected with influenza virus A/Fukuoka/C29/85 (H3N2) before 14 days were secondary infected with A/PR/8 virus and administered orally with SST (1 g/kg, 5 times) from 2 h to 5 days after the secondary infection, replication of the virus in both nasal and broncho-alveolar cavities were significantly inhibited at 5 days after the secondary infection in comparison with water-treated control. Oral administration of SST (1 g/kg, 18 times) from 7 days before to 14 days after vaccination followed by secondary nasal inoculation of influenza HA vaccine (5 micrograms/mouse) at 14 days after the first vaccination significantly augmented nasal antiviral IgA antibody and broncho-alveolar and serum antiviral IgG antibodies. These results suggest that SST is useful for influenza virus infection on aged persons and for cross-protection of subtypes of influenza A viruses and influenza B virus. SST is also useful for the treatment of influenza virus infection on human which has a history of influenza virus infection and/or influenza vaccination.

Aging↗
PubMed2000

Adaptive mutations in Sindbis virus E2 and Ross River virus E1 that allow efficient budding of chimeric viruses.

Alphavirus glycoproteins E2 and E1 form a heterodimer that is required for virus assembly. We have studied adaptive mutations in E2 of Sindbis virus (SIN) and E1 of Ross River virus (RR) that allow these two glycoproteins to interact more efficiently in a chimeric virus that has SIN E2 but RR E1. These mutations include K129E, K131E, and V237F in SIN E2 and S310F and C433R in RR E1. Although RR E1 and SIN E2 will form a chimeric heterodimer, the chimeric virus is almost nonviable, producing about 10(-7) as much virus as SIN at 24 h and 10(-5) as much after 48 h. Chimeras containing one adaptive change produced 3 to 20 times more virus than did the parental chimera, whereas chimeras with two changes produced 10 to 100 times more virus and chimeras containing three mutations produced yields that were 180 to 250 times better. None of the mutations had significant effects upon the parental wild-type viruses, however. Passage of the triple variants eight or nine times resulted in variants that produced virus rapidly and were capable of producing >10(8) PFU/ml of culture fluid within 24 h. These further-adapted variants possessed one or two additional mutations, including E2-V116K, E2-S110N, or E1-T65S. The RR E1-C433R mutation was studied in more detail. This Cys is located in the putative transmembrane domain of E1 and was shown to be palmitoylated. Mutation to Arg-433 resulted in loss of palmitoylation of E1. The positively charged arginine residue within the putative transmembrane domain of E1 would be expected to alter the conformation of this domain. These results suggest that interactions within the transmembrane region are important for the assembly of the E1/E2 heterodimer, as are regions of the ectodomains possibly identified by the locations of adaptive mutations in these regions. Further, the finding that four or five changes in the chimera allow virus production that approaches the levels seen with the parental SIN and exceeds that of the parental RR illustrates that the structure and function of SIN and RR E1s have been conserved during the 50% divergence in sequence that has occurred.

Adaptation, Physiological↗
PubMed1996

Different patterns of cytokine induction in cultures of respiratory syncytial (RS) virus-specific human TH cell lines following stimulation with RS virus and RS virus proteins.

Human peripheral blood mononuclear cell (PBMC) proliferative responses to live respiratory syncytial (RS) virus, formalin-inactivated RS (Fl-RS) virus, RS virus F (fusion) protein, and RS virus G (attachment) protein were assessed. All donors responded to challenge with whole RS virus antigens and F and G proteins. F protein responses elicited higher levels of response than equivalent concentrations of G protein in nine out of ten adult RS-seropositive donors. Stimulation of PBMC induced low levels of interleukin 2 (IL-2), interferon gamma (IFN-gamma), IL-4, and IL-10 production. Human RS virus-specific T cell lines were generated from peripheral blood cultures following in vitro stimulation with RS virus antigens. All lines generated were shown to be MHC class II restricted. Characterisation of the lines was carried out by determining the levels of IL-2, IFN-gamma, IL-4, and IL-10 in culture supernatants. T cell lines enriched for RS virus-specific cells provided a more sensitive system than PBMC cultures for the detection of cytokines. The pattern of cytokine production varied for the individual lines, and the detection of TH1 and TH2 cytokines was dependent on the nature of the stimulating RS virus antigen. Live RS virus induced a TH1 pattern of cytokines (IL-2 and IFN-gamma), whereas FI-RS virus induced the production of both TH1 and TH2 cytokines. In addition, TH lines specific for individual RS virus proteins produced different cytokine profiles. F protein-specific lines generated TH1-type cytokines (IL-2 and IFN-gamma), whereas G protein-specific lines generated TH2-type cytokines (IL-4 and IL-10).

Adult↗
PubMed2002

Characterization and identification of Oya virus, a Simbu serogroup virus of the genus Bunyavirus, isolated from a pig suspected of Nipah virus infection.

A virus, named Oya virus, was isolated in Vero cell cultures from the lungs of a pig suspected of Nipah virus infection. The virus was revealed as a spherical enveloped RNA virus with a diameter of 79 nm. For identification of Oya virus, RT-PCR was performed. A common primer set for S-RNA of the Simbu serogroup of the genus Bunyavirus was able to amplify a cDNA from Oya virus RNA. The sequence data of the product revealed that the partial gene of Oya virus S-RNA segment had 65-70% homology with published cDNA sequences of Simbu serogroup viruses. The phylogenetic analysis of the data showed that the Oya virus is grouped in Simbu serogroup, but is genetically distinct from the serogroup viruses that have been analyzed molecularly. Serological surveys revealed that the virus distributed widely and densely in Malaysia.

Animals↗
PubMed1983

Naturally occurring leukemia viruses in H-2 congenic C57BL mice. III. Characterization of C-type viruses isolated from lymphomas induced by milk transmission of B-ecotropic virus.

The prevalence of different host-range classes of murine leukemia virus (MuLV) was studied in C57BL mice with (V+) and without (V-) milk transmission of a naturally occurring B-tropic ecotropic MuLV. Virus isolates were studied with respect to growth properties, XC-plaque formation, antigen profiles of their envelope proteins (gp70 and P15(E)), gp70 tryptic-peptide maps, and their potential to induce lymphomas after inoculation into newborn mice. B-tropic ecotropic MuLV with the capacity to cause plaques in XC cells was isolated from almost all lymphomas of both V+ and V- sublines. The reaction patterns of these ecotropic isolates with monoclonal antibodies reactive with MuLV-env proteins and the tryptic-peptide maps of the gp70 molecule indicate that they are similar to each other and differ only slightly from the ecotropic MuLV in the spleens of young V+ animals, which is identical to the milk-transmitted virus. XC-, B-tropic dualtropic mink cell focus-inducing (MCF) viruses were isolated from the majority of different types of lymphoma (B cell, T cell, or neither B nor T cell derived), but not from the spleens or milk of young V+ or V- animals. The env proteins of the MCF isolates are highly heterogeneous, but most isolates originating from B10.AV + T-cell lymphomas share MCF-related epitopes in their gp85 envelope precursor with AKR MCF-247 virus. Most MCF viruses isolated from non-T lymphomas do not possess these epitopes. The results indicate that also in this model the generation of dualtropic MCF viruses might be important in lymphoma induction, although only some of the cloned MCF viruses show enhanced oncogenic properties in comparison with ecotropic isolates. A cloned oncogenic MCF virus induced different lymphoma types in C57BL/10 (= B10, H-2b) and B10.A (H-2a) mice, similar to what was found earlier with the milk-transmitted virus. Hence, the lymphoma-type differences are not due to differences in the B-tropic ecotropic viruses transmitted through the milk in these strains, but reflect an influence of the H-2 complex on the phenotype of the virus-induced lymphomas.

Animals↗
PubMed1989

RB virus: a strain of Friend virus that produces a 'Friend virus-like' disease in Fv-2rr mice.

RB virus is a newly derived strain of Friend virus that was adapted to produce a 'Friend-like' disease in mice that are genetically resistant to wild-type Friend virus. RB virus was produced by passing high titers of the wild-type Friend virus (Lilly-Steeves polycythemia-producing strain) through adult Fv-2rr mice. Titration of the defective spleen focus-forming virus indicated RB virus infected similar numbers of Fv-2ss or Fv-2rr target cells. Analysis of the spleens from mice infected with RB virus indicated that RB induced the early stage of Friend disease (erythroid proliferation) in both Fv-2rr and Fv-2ss mice. Fv-2ss mice infected with RB virus developed the classical Friend disease within 3 weeks. In contrast, the percentage of Fv-2rr mice developing the 'Friend-like' disease after infection with RB virus never exceeded 60%. The latency period of RBV in Fv-2rr mice was strain dependent. D2.R16 (Fv-2rr) developed the syndrome more rapidly than C57BL/6 (Fv-2rr). RB virus retained the capacity to transform erythroprogenitor cells from both Fv-2ss and Fv-2rr animals. Cells infected with RB virus consistently produced a modified SFFV envelope protein, gp48.

Animals↗
PubMed1981

New cell surface gp70 related to Friend mink cell focus-inducing virus is expressed on Friend virus-induced erythroleukemic spleen cells after elimination of ecotropic Friend virus gp70 in Rfv-3r/s mice.

Spleen cells from Rfv-3r/s mice with Friend virus-induced erythroleukemia were analyzed for expression of virus-induced proteins with monoclonal antiviral antibodies and conventional antisera. Leukemic spleen cells, 30-60 d after virus inoculation, expressed decreased amounts of ecotropic Friend murine leukemia helper virus gag- and env-encoded cell surface and intracellular proteins compared with leukemic cells tested 8-10 d after virus inoculation. In contrast, the spleen focus-forming virus-induced protein, gp55, was present on both leukemia cell populations. This difference appeared to be mediated by the humoral antibody response in Rfv-3r/s mice, which could recognize only ecotropic gag and env proteins, and not gp55. A new gp70 molecule cross-reactive with a recombinant Friend mink cell focus-inducing virus was found in large quantities on late leukemic cells. This protein appeared to be derived from a recombinant virus produced during the course of Friend virus infection. The appearance of this new gp70 suggests that recombinant viruses other than spleen focus-forming virus may play a role in Friend virus-induced erythroleukemia.

Animals↗
PubMed1984

Protection of mice infected with a lethal dose of Semliki Forest virus by defective interfering virus: modulation of virus multiplication.

Certain defective interfering (DI) Semliki Forest virus (SFV) preparations completely protected the majority of mice inoculated with a normally lethal dose of SFV, and the surviving mice showed no signs of disease during the period of observation. Depending upon which DI SFV preparation was used, the survivors were resistant to challenge with 100 LD50 SFV (DI SFV p13a), or were completely sensitive (DI SFV p4), the latter having evidently failed to establish a protective immunity. In this report we compared the ability of these two DI SFV preparations to inhibit multiplication of infectious virus in mice inoculated with 10 LD50 SFV. The following conclusions emerged: virus multiplication was profoundly inhibited in the majority of mice treated with either of the DI virus preparations although there was significant multiplication in most tissues, including brain. The number of mice showing evidence of reduced infectivity titres (58%) correlated well with the 60% which survived without disease in lethality experiments. Despite the presence of infectivity, no SFV antigen or histopathological lesions were detected in brain or spinal cord. The DI virus preparations p4 and p13a altered the distribution of infectivity in the mouse in different ways: during the first 2 days of the infection modulated by DI virus p4, the infectivity titres (in brain, olfactory lobes and spleen) were comparatively high, being greater than 1% of those in mice inoculated with standard virus alone. However, from day 3, titres declined precipitously and there was little infectivity in any of the tissues investigated. On the other hand, mice treated with DI SFV p13a had, over the entire duration of infection, greatly reduced though significant infectivity in brain, olfactory lobes and spleen and very little infectivity in serum. In a minority of mice (14.5%), DI virus p13a altered the distribution of infectivity between different tissues so that there was significantly decreased virus in just one or two of the four tissues investigated, suggesting that the infection was being subtly modulated by the DI virus. Interference assays failed to detect DI SFV in any tissue samples although the effects of DI virus on infection in the mouse were obvious.

Animals↗