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At least 127 records · Page 7Linked to original sources
PubMed2004

SEN virus does not affect treatment response in hepatitis C virus coinfected patients but SEN virus response depends on SEN virus DNA concentration.

AIM: To clarify the effect of SEN virus (SENV) infection on a combination therapy including interferon alfa (IFN-alpha) or pegylated-IFN with ribavirin in patients with chronic hepatitis and the effect of a combination therapy on SENV. METHODS: SENV DNA was determined by polymerase chain reaction in serum samples from 95 patients with chronic hepatitis C. Quantitative analysis was done for SENV H DNA. RESULTS: Twenty-one (22%) of 95 patients were positive for SENV DNA. There was no difference in clinical and biochemical parameters between patients with HCV infection alone and coinfected patients. The sustained response rate for HCV clearance after combination therapy did not differ between patients with SENV (52%) and without SENV (50%, n.s.). SENV DNA was undetectable in 76% of the initially SENV positive patients at the end of follow-up. SENV H response to combination therapy was significantly correlated with SENV DNA level (P=0.05). CONCLUSION: SENV infection had no influence on the HCV sustained response rate to the combination therapy. Response rate of SENV to the combination therapy depends on SENV DNA level.

Adult↗
PubMed1995

Construction of human immunodeficiency virus 1/simian immunodeficiency virus strain mac chimeric viruses having vpr and/or nef of different parental origins and their in vitro and in vivo replication.

We constructed a series of human immunodeficiency virus 1 (HIV-1)/simian immunodeficiency virus strain mac (SIVmac) chimeric viruses having vpr and/or nef genes of either HIV-1 or SIVmac based on a chimeric virus with LTRs, gag, pol, vif and vpx derived from SIVmac and tar, rev, vpu and env from HIV-1. All of the chimeric viruses replicated in human and macaque peripheral blood mononuclear cells (PBMCs) and in several CD4+ human cell lines, though their growth potentials were slightly different depending on whether vpr and nef were from HIV-1 or SIVmac, or were defective. The presence of nef accelerated replication in all the cells used and the replication of each chimera appeared to reflect that of the parental virus from which nef was derived. The presence of vpr had no clear effect in human and monkey PBMCs, but the replication of each chimera was influenced by the origin of vpr in H9 and A3.01 cells. NM-3rN, which carries HIV-1 vpr and SIVmac nef, was inoculated intravenously into three rhesus monkeys, three cynomolgus monkeys and two pig-tailed monkeys. From 2 to 14 weeks after inoculation, viruses were consistently re-isolated from all the monkeys and virus loads were as high as that of SIVmac reported previously. The results indicate that infection with NM-3rN is more efficient than any of our previous chimeric viruses and suggest that NM-3rN, having HIV-1 Env, will be a useful challenge virus for evaluating AIDS vaccines based on HIV-1 Env in macaque monkeys instead of chimpanzees.

Animals↗
PubMed2004

Rapid and sensitive method using multiplex real-time PCR for diagnosis of infections by influenza a and influenza B viruses, respiratory syncytial virus, and parainfluenza viruses 1, 2, 3, and 4.

Laboratory diagnosis of viral respiratory infections is generally performed by virus isolation in cell culture and immunofluorescent assays. Reverse transcriptase PCR is now recognized as a sensitive and specific alternative for detection of respiratory RNA viruses. A rapid real-time multiplex PCR assay was developed for the detection of influenza A and influenza B viruses, human respiratory syncytial virus (RSV), parainfluenza virus 1 (PIV1), PIV2, PIV3, and PIV4 in a two-tube multiplex reaction which used molecular beacons to discriminate the pathogens. A total of 358 respiratory samples taken over a 1-year period were analyzed by the multiplex assay. The incidence of respiratory viruses detected in these samples was 67 of 358 (19%) and 87 of 358 (24%) by culture and real-time PCR, respectively. Culture detected 3 influenza A virus, 2 influenza B virus, 57 RSV, 2 PIV1, and 2 PIV3 infections. All of these culture-positive samples and an additional 5 influenza A virus, 6 RSV, 2 PIV1, 1 PIV2, 1 PIV3, and 3 PIV4 infections were detected by the multiplex real-time PCR. The application of real-time PCR to clinical samples increases the sensitivity for respiratory viral diagnosis. In addition, results can be obtained within 6 h, which increases clinical relevance. Therefore, use of this real-time PCR assay would improve patient management and infection control.

Cell Line↗
PubMed2001

Release of virus from lymphoid tissue affects human immunodeficiency virus type 1 and hepatitis C virus kinetics in the blood.

Kinetic parameters of human immunodeficiency virus type 1 (HIV-1) and hepatitis C virus (HCV) infections have been estimated from plasma virus levels following perturbation of the chronically infected (quasi-) steady state. We extend previous models by also considering the large pool of virus localized in the lymphoid tissue (LT) compartment. The results indicate that the fastest time scale of HIV-1 plasma load decay during therapy probably reflects the clearance rate of LT virus and not, as previously supposed, the clearance rate of virus in plasma. This resolves the discrepancy between the clearance rate estimates during therapy and those based on plasma apheresis experiments. In the extended models plasma apheresis measurements are indeed expected to reflect the plasma decay rate. We can reconcile all current HIV-1 estimates with this model when, on average, the clearance rate of virus in plasma is approximately 20 day(-1), that of LT virus is approximately 3 day(-1), and the death rate of virus-producing cells is approximately 0.5 day(-1). The fast clearance in the LT compartment increases current estimates for total daily virus production. Because HCV is produced in the liver, we let virus be produced into the blood compartment of our model. The results suggest that extending current HCV models with an LT compartment is not likely to affect current estimates for kinetic parameters and virus production. Estimates for treatment efficacy might be affected, however.

Anti-HIV Agents↗
PubMed2001

Identification of equine herpesvirus 3 (equine coital exanthema virus), equine gammaherpesviruses 2 and 5, equine adenoviruses 1 and 2, equine arteritis virus and equine rhinitis A virus by polymerase chain reaction.

OBJECTIVE: To develop rapid (< 8 hour) tests using polymerase chain reaction (PCR) for the diagnosis of equine herpesvirus 3 (EHV3; equine coital exanthema virus), equine gammaherpesviruses 2 (EHV2) and EHV5, equine adenovirus 1 (EAdV1), EAdV2, equine arteritis virus (EAV), equine rhinitis A virus (ERAV; formerly equine rhinovirus 1) DESIGN: Either single round or second round (seminested) PCRs were developed and validated. METHODS: Oligonucleotide primers were designed that were specific for each virus, PCR conditions were defined and the specificity and sensitivity of the assays were determined. The application of the tests was validated using a number of independent virus isolates for most of the viruses studied. The PCRs were applied directly to clinical samples where samples were available. RESULTS: We developed a single round PCR for the diagnosis of EHV3, a seminested PCR for EHV2 and single round PCRs for EHV5, EAdV1, EAdV2 and RT-PCRs for EAV and ERAV. The PCR primer sets for each virus were designed and shown to be highly specific (did not amplify any recognised non-target template) and sensitive (detection of minimal amounts of virus) and, where multiple virus isolates were available all isolates were detected. CONCLUSION: The development and validation of a comprehensive panel of PCR diagnostic tests, predominantly for viruses causing equine respiratory disease, that can be completed within 8 hours from receipt of clinical samples, provides a major advance in the rapid diagnosis or exclusion diagnosis of these endemic equine virus diseases in Australia.

Adenoviridae↗
PubMed1980

Temperature-sensitive mutants of influenza A virus: transfer of the two temperature-sensitive lesions in the Udorn/72-ts-1A2 virus to the A2Hong Kong/123/77 (H1N1) wild-type virus.

The influenza A/Udorn/72-ts-1A2 virus possesses temperature-sensitive mutations in the genes coding for the P1 and P3 polymerase proteins. It is being evaluated as a donor of its attenuating temperature-sensitive genes to produce recombinant live vaccine strains of epidemic variants of influenza A virus. Transfer of the P1 and P3 genes to two viruses within the H3N2 subtype of influenza A virus (i.e., the A/Victoria/3/75 and A/Alaska/6/77 viruses) conferred on each variant the following properties: (i) 37 degrees C shutoff temperature for plaque formation, (ii) almost complete restriction of viral replication in the lungs, (iii) a 100-fold restriction of viral replication in the nasal turbinates, and (iv) genetic stability after replication in hamsters. This study was undertaken to determine whether the transfer of the two ts-1A2 temperature-sensitive genes into a virus belonging to the H1N1 subtype (i.e., the A/Hong Kong/123/77 virus) would result in a restriction of replication in vitro and in vivo comparable to that observed with the previously studied H3N2 recombinant viruses in hamsters. This was found to be the case. In addition, infection of hamsters with the A/Hong Kong/77-ts-1A2 virus induced significant resistance to infection with wild-type A/Hong Kong/77 virus. Thus, the two ts-1A2 temperature-sensitive genes attenuated influenza A viruses belonging to two distinct subtypes to a specific and predictable level. An unexpected genetic interaction was observed between several A/Hong Kong/77-ts-1A2 segregants bearing the group 5 (P1) temperature-sensitive lesion. One interpretation of these results is that intracistronic complementation occurred between these segregants.

Animals↗
PubMed2005

Prevention of virus persistence and protection against immunopathology after Borna disease virus infection of the brain by a novel Orf virus recombinant.

The Parapoxvirus Orf virus represents a promising candidate for novel vector vaccines due to its immune modulating properties even in nonpermissive hosts such as mouse or rat. The highly attenuated Orf virus strain D1701 was used to generate a recombinant virus (D1701-VrVp40) expressing nucleoprotein p40 of Borna disease virus, which represents a major antigen for the induction of a Borna disease virus-specific humoral and cellular immune response. Infection with Borna disease virus leads to distinct neurological symptoms mediated by the invasion of activated specific CD8+ T cells into the infected brain. Usually, Borna disease virus is not cleared from the brain but rather persists in neural cells. In the present study we show for the first time that intramuscular application of the D1701-VrVp40 recombinant protected rats against Borna disease, and importantly, virus clearance from the infected brain was demonstrated in immunized animals. Even 4 and 8 months after the last immunization, all immunized animals were still protected against the disease. Initial characterization of the immune cells attracted to the infected brain areas suggested that D1701-VrVp40 mediated induction of B cells and antibody-producing plasma cells as well as T cells. These findings suggest the induction of various defense mechanisms against Borna disease virus. First studies on the role of antiviral cytokines indicated that D1701-VrVp40 immunization did not lead to an enhanced early response of gamma or alpha interferon or tumor necrosis factor alpha. Collectively, this study describes the potential of the Orf virus vector system in mediating long-lasting, protective antiviral immunity and eliminating this persistent virus infection without provoking massive neuronal damage.

Animals↗
PubMed2004

Population-based surveillance for hospitalizations associated with respiratory syncytial virus, influenza virus, and parainfluenza viruses among young children.

OBJECTIVE: Respiratory syncytial virus (RSV), influenza virus, and parainfluenza viruses (PIV) cause significant morbidity in young children. Although only influenza virus infection and illness is currently vaccine-preventable, vaccines are under development for RSV and PIV. We established a prospective, active population-based surveillance network to provide precise estimates of hospitalization rates for viral acute respiratory illness (ARI) in young children and to measure the potential impact of enhanced vaccine usage on these rates. METHODS: Prospective, active population-based surveillance was conducted in young children who were hospitalized for ARI from October 1, 2000, to September 30, 2001, in Monroe County, New York (Rochester area) and Davidson County, Tennessee (Nashville area). Eligible children younger than 5 years were those who resided in surveillance counties and were hospitalized for febrile or acute respiratory illness. Viral culture and polymerase chain reaction identified viruses from nasal and throat samples obtained from all surveillance children. We measured population-based rates of hospitalization for RSV, influenza virus, and PIV as well as demographic, clinical, and risk factor assessment for each virus. RESULTS: Of 812 eligible hospital admissions, 592 (73%) children were enrolled. Of the enrolled children, RSV was identified in 20%, influenza in 3%, PIV in 7%, other respiratory viruses in 36%, and no detectable virus in 39%. Population-based rates of ARI hospitalizations in children younger than 5 years were 18 per 1000. Virus-positive hospitalization rates per 1000 children were 3.5 for RSV, 1.2 for PIV, and 0.6 for influenza virus. Younger age (particularly <1 year), black and Hispanic race/ethnicity, male gender, and presence of chronic underlying illness were associated with higher hospitalization rates. CONCLUSIONS: This study confirms that children younger than 5 years and particularly children younger than 1 year have a high burden of hospitalization from RSV, influenza, and PIV. The enhanced use of influenza vaccine and the development of RSV and PIV vaccines have the potential to reduce markedly the pediatric morbidity from ARIs.

Age Distribution↗
PubMed1992

The distribution of Challenge virus standard rabies virus versus skunk street rabies virus in the brains of experimentally infected rabid skunks.

The proposal that the bizarre behavioral changes which occur during rabies infection are due to selective infection of limbic system neurons was further studied in skunks (a species important in naturally occurring disease). A detailed immunohistochemical study of brains of skunks experimentally infected with either Challenge virus standard (CVS) or street rabies virus revealed only trace amounts of viral antigen in many limbic system neurons and marked differences in viral distribution between street and CVS virus. These data were collected during early stage rabies when behavioral changes occur. Areas which contained heavy accumulations of street rabies virus but low amounts of CVS rabies virus were the neuronal perikarya and processes of the dorsal motor nucleus of the vagus, midbrain raphe, hypoglossal and red nuclei. In contrast, large accumulations of CVS virus were found in the Purkinje cells of the cerebellum, the habenular nuclei and in pyramidal cells throughout the cerebral cortex, while corresponding areas in all street virus-infected skunks contained minimal antigen. These findings were very consistent for animals of the same experimental group and between skunks inoculated both intramuscularly and intranasally with skunk street virus. Skunks inoculated intramuscularly with CVS rabies virus failed to develop rabies. Since, in this model, street virus infection generally produces furious rabies and CVS infection results in dumb rabies, we speculate that the behavioral changes which occur in these two different clinical syndromes are due to the heavy and specific accumulation of virus in different regions of the CNS. These results show that regions other than those of the limbic system may also be involved in the pathogenesis of behavior changes in rabid animals.

Animals↗
PubMed1956

Studies on host-virus interactions in the chick embryo-influenza virus system. XIII. Some aspects of non-infectious virus production.

Certain aspects of the formation of non-infectious hemagglutinins (NIHA) in the chick embryo infected with influenza virus have been analyzed. It was shown by the use of combined in ovo-deembryonation technics that little or no NIHA is released following infection with small doses of standard virus during the most active and constant growth periods of the virus extending to about the 36th hour of incubation in spite of the fact that multiple infection of cells must have taken place in the latter half of that period. A slight decrease in the ID(50)/HA ratios of the yields obtained after the 36th hour, coinciding with the falling off of virus production and release may possibly be explained in terms of inactivation of completed virus or leakage of as yet incompleted virus from damaged cells. Exposure of the entodermal cells of the allantois of eggs deembryonated shortiy after injection of saturation or near saturation inocula of standard seed to large quantities of infectious virus added to the media at various times after infection and not extending over more than 2 hours resulted in a decrease of the ID(50)/HA ratios of the progenies only during the first 2 or possibly 4 hours after the primary inoculation. Later addition did not influence the yields. As discussed, such sudden and heavy exposures of cells are not expected to occur during the infectious process induced by small inocula of standard seed. The possible role of destruction of cell receptors in NIHA production has been analyzed in several ways. The addition of receptor-destroying enzyme (RDE) to the media of deembryonated eggs after near saturation inocula of standard seeds, if anything, increased the ID(50)/HA ratios of the progenies, and that only when added during the first few hours following infection, presumably by reducing the changes for high multiplicity of infection of cells. In contrast, ultraviolet-inactivated virus, which retains its enzymatic activity, lowered, if anything, the ID(50)/HA ratios of the progenies, when present in the media of deembryonated eggs from the 2nd to 4th or possibly 6th hour after infection. Excessive amounts of irradiated virus may still cause some degree of interference under these conditions. Later addition of irradiated viruses were without effect with respect to NIHA production or interference. In attempts to alter the cell receptors prior to infection by potassium periodate (KIO(4)), it was noted that the addition of glycerol led to the appearance and partial retention for at least 24 hours of substances in the allantoic fluids which were capable of inactivating considerable proportions of standard virus. These data indicate that destruction of external cell receptors plays little if any role in NIHA production. The implications of these findings are discussed.

Hemagglutination↗
PubMed1994

Detection of immunoglobulin M (IgM), IgA, and IgG Norwalk virus-specific antibodies by indirect enzyme-linked immunosorbent assay with baculovirus-expressed Norwalk virus capsid antigen in adult volunteers challenged with Norwalk virus.

Pre- and postexposure sera collected from 17 adult volunteers challenged with Norwalk virus as described previously (D. Y. Graham, X. Jiang, T. Tanaka, A. Opekun, P. Madore, and M. K. Estes, J. Infect. Dis. 170:34-43, 1994) were examined for Norwalk virus-specific immunoglobulin M (IgM), IgA, and IgG by indirect enzyme-linked immunosorbent assays with recombinant Norwalk virus antigen bound to the solid phase. Sixteen of the 17 volunteers had evidence of past infection, all presenting with preexisting IgG antibody of high avidity; only one volunteer had no evidence of previous infection. Virus infection was detected in 14 of the 16 volunteers with evidence of past infection, and 9 of the infected volunteers had symptomatic illness. A significant rise in both virus-specific IgA and IgG titers was detected after challenge in all of the volunteers who became ill. Five of the asymptomatic volunteers who were infected had rising titers of virus-specific IgG, but only two of the five had a concomitant rise in their virus-specific IgA antibody titers. Antibody rises were detectable in eight of nine ill volunteers 8 to 11 days after challenge but in the asymptomatic volunteers only after more than 15 days had elapsed. Virus-specific IgM was detected after challenge in all 14 infected volunteers. Between symptomatic and asymptomatic volunteers there were no significant differences in titers of virus-specific IgG and IgA in serum before challenge; however, there were significantly higher titers in symptomatic volunteers between 8 and > 90 days after challenge for virus-specific IgG and 8 and 24 days after challenge for virus-specific IgA.

Adult↗
PubMed1998

Common themes of antibody maturation to simian immunodeficiency virus, simian-human immunodeficiency virus, and human immunodeficiency virus type 1 infections.

Characterization of virus-specific immune responses to human immunodeficiency virus type 1 (HIV-1) and simian immunodeficiency virus (SIV) is important to understanding the early virus-host interactions that may determine the course of virus infection and disease. Using a comprehensive panel of serological assays, we have previously demonstrated a complex and lengthy maturation of virus-specific antibody responses elicited by attenuated strains of SIV that was closely associated with the development of protective immunity. In the present study, we expand these analyses to address several questions regarding the nature of the virus-specific antibody responses to pathogenic SIV, SIV/HIV-1 (SHIV), and HIV-1 infections. The results demonstrate for the first time a common theme of antibody maturation to SIV, SHIV, and HIV-1 infections that is characterized by ongoing changes in antibody titer, conformational dependence, and antibody avidity during the first 6 to 10 months following virus infection. We demonstrate that this gradual evolution of virus-specific antibody responses is independent of the levels of virus replication and the pathogenicity of the infection viral strain. While the serological assays used in these studies were useful in discriminating between protective and nonprotective antibody responses during evaluation of vaccine efficacy with attenuated SIV, these same assays do not distinguish the clinical outcome of infection in pathogenic SIV, SHIV, or HIV-1 infections. These results likely reflect differences in the immune mechanisms involved in mediating protection from virus challenge compared to those that control an established viral infection, and they suggest that additional characteristics of both humoral and cellular responses evolve during this early immune maturation.

Animals↗
PubMed2003

DNA immunization with hepatitis C virus (HCV) polycistronic genes or immunization by HCV DNA priming-recombinant canarypox virus boosting induces immune responses and protection from recombinant HCV-vaccinia virus infection in HLA-A2.1-transgenic mice.

We studied immune responses to hepatitis C virus (HCV) genes delivered as DNA encoding the entire HCV protein coding genome in two polycistronic plasmids encoding HCV capsid-E1-E2-NS2-NS3 and HCV NS3-NS4-NS5 in HLA-A2.1-transgenic mice. Immune responses to HCV DNA prime and recombinant canarypox virus boost were also studied with the above constructs. At 8 weeks after a canarypox virus boost, the DNA prime/canarypox virus boosting regimen induced potent cellular immune responses to HCV structural and nonstructural proteins on target cells expressing the HLA-A2.1 allele. High frequencies of gamma interferon-secreting cells, as detected by enzyme-linked immunospot assay, were obtained in response to several endogenously expressed HCV proteins. We also observed cytotoxic-T-lymphocyte reactivity in response to endogenously expressed HCV proteins in fresh spleen cells without in vitro expansion. Upon challenge with a recombinant vaccinia virus expressing HCV proteins at 2 months postimmunization, the HCV DNA prime/canarypox virus-immunized mice showed a complete reduction in vaccinia virus titers compared to HCV DNA prime/boost- and mock-immunized controls. Immune responses were still detectable 4 months after canarypox virus boost in immunized mice. Interestingly, at 10 months postimmunization (8 months after canarypox virus boost), the protection in HCV DNA prime/boost-immunized mice against recombinant HCV-vaccinia virus challenge was higher than that observed in HCV DNA prime/canarypox virus boost-immunized mice.

Animals↗
PubMed2000

Coevolution of host and virus: cellular localization of virus in myxoma virus infection of resistant and susceptible European rabbits.

The coevolution of myxoma virus and the wild European rabbit in Australia and the development of resistance to myxomatosis in wild rabbits have been well described. However, the mechanism of resistance to myxomatosis in wild rabbits is not understood. To determine the basis of resistance, the pathogenesis of the virulent standard laboratory strain (SLS) and the attenuated Uriarra (Ur) strain of myxoma virus were examined in Australian wild rabbits that have been naturally selected in the field for resistance to myxomatosis and in laboratory rabbits which have never been selected for resistance. Virus was localized in tissue sections by immunofluorescence. In all cases virus antigen was initially present in dendritic cells of the dermis before localizing predominantly to the epidermis by Day 6. Antigen-containing cells were detected in the lymph nodes by 24 h after inoculation. Virus replication occurred predominantly in T lymphocytes of the paracortex but SLS also replicated in germinal centers. SLS replication induced loss of most lymphocytes from the lymph nodes of susceptible rabbits. Apoptosis of lymphocytes within the lymph nodes was a major feature of all infections. These apoptotic cells did not contain detectable viral antigen but were often adjacent to infected cells. Ongoing apoptosis of lymphocytes within lymph nodes was also a feature of the recovery phase when very few or no virus-infected cells could be detected. Differences between virulent and attenuated viruses in the wild and laboratory rabbits were predominantly in the degree of tissue pathology in the draining lymph node and distal lymph node and in the type of inflammatory responses, particularly in the skin. SLS infection of laboratory rabbits was associated with a very mild inflammatory response, often distant from the site of virus replication and comprised predominantly of neutrophils. In contrast, Ur-infected rabbits and SLS-infected wild rabbits had an intense inflammatory response adjacent to the site of virus replication and this was comprised predominantly of mononuclear cells. Both the initial infection of dendritic cells and the ongoing destruction of lymphocytes provide obvious mechanisms for the suppression of the immune response by myxoma virus.

Animals↗
PubMed1989

Rescue of Sendai virus from viral ribonucleoprotein-transfected cells by infection with recombinant vaccinia viruses carrying Sendai virus L and P/C genes.

The Sendai virus ribonucleoprotein (RNP) showed only very low plaque-forming titers upon transfection and the virus yields after one-step growth were quite limited. We tried to enhance the Sendai virus yield by supplying the viral L and P/C gene products through vaccinia vectors. A combination of the recombinant vaccinia viruses carrying the L gene (Vac-HL) and the P/C gene (Vac-HPC), both of which were driven by the promoter of the vaccinia virus 7.5K protein gene, enhanced the yield only a little whereas another combination of Vac-HLd7.5, the L gene insert of which was driven by the promoter of the vaccinia virus thymidine kinase gene in place of the 7.5K promoter, and Vac-HPC greatly enhanced the Sendai virus yield. This seemed to correlate with the fact that the Vac-HL interfered with Sendai virus growth markedly while the Vac-HLd7.5 did not. These results strongly suggest that the L and P/C gene products act in cooperation as the RNA polymerase, and overproduction of the L protein is inhibitory for Sendai virus growth. This system seems to be of value as a tool for analyzing the functions of L and P/C genes of Sendai virus.

Animals↗
PubMed1978

The entry into host cells of Sindbis virus, vesicular stomatitis virus and Sendai virus.

We have compared the mechanisms of entry into host cells of three enveloped viruses: Sendai virus, vesicular stomatitis virus (VSV) and Sindbis virus. Virus entry by membrane fusion should antigenically modify the surface of a newly infected cell in such a way that it will be killed by anti-viral antibody and complement. On the other hand, virus entry by a mechanism involving uptake by the cell of the whole virion should not make cells sensitive to antibody and complement. As expected, cells newly infected with Sendai virus were readily and completely lysed by anti-Sendai antibody and complement. In marked contrast, however, cells newly infected with either Sindbis virus or VSV were killed by anti-viral antibody and complement only when infected at an extremely high multiplicity of infection, in excess of 1000 plaque-forming units per cell. We favor the following explanation for these results with Sindbis virus and VSV: a very large majority of the Sindbis and VSV virions entered the infected cells by some means other than membrane fusion, presumably engulfment of the whole particle. Efficient entry by way of membrane fusion may therefore not be a general characteristic of enveloped viruses.

Antigens, Surface↗
PubMed1984

Characterization of the genotype and level of attenuation of an influenza A reassortant virus produced by mating the Xia-ts donor virus with A/Beijing/70 (H1N1) wild type virus.

Two H1N1 progeny viruses derived by mating the attenuated donor virus, the A/Ningxia/72-ts (H3N2), and the A/Beijing/70 (H1N1) wild type virus were characterized for their genotype and their level of attenuation in susceptible adult volunteers. One progeny virus, clone PX62, was not a reassortant since it received each of its eight RNA segments from the H1N1 wild type virus. THis virus caused febrile influenza illness. Another progeny virus, clone PXH107, was a reassortant which received the genes coding for the surface antigens from the H1N1 parent virus but each of the other six RNA segments from the H3N2 parent virus. This clone was satisfactorily attenuated in susceptible adults and induced an immune response in at least 60% of the vaccinees. These results indicate that the genetic determinants of attenuation of the A/Ningxia/72-ts virus reside on one or more of the RNA segments that do not code for the surface antigens.

Adolescent↗
PubMed1991

Anamnestic immune response of pigs to pseudorabies virus: latent virus reactivation versus direct oronasal and parenteral exposure to virus.

The humoral antibody response of pseudorabies-immune pigs to reactivation of latent pseudorabies virus (PRV) was compared with the response following direct exposure to virulent PRV. Nine pigs that had been vaccinated for pseudorabies and later exposed to virulent virus to establish latent infection were given dexamethasone to reactivate latent virus (3 pigs), were exposed oronasally and parenterally to virulent virus (3 pigs), or were kept as nontreated controls (3 pigs). Sera collected from all 9 pigs just before and 3 weeks after treatment were tested by virus neutralization and radioimmunoprecipitation. The 3 pigs exposed directly to virulent virus and 2 of the 3 pigs given dexamethasone had a 4-fold or greater increase in neutralizing antibody titer. All 6 of these pigs had an increase in precipitating antibody activity. Precipitation patterns changed both quantitatively and qualitatively, especially for virus-coded proteins of relatively low molecular weight (less than 46 K). There were some differences in the precipitation patterns associated with sera of individual pigs. However, there was no clear indication of any difference between the 2 treatment groups and therefore no evidence that reactivation of latent virus is associated with any unique immunologic response that could be detected by radioimmunoprecipitation and used diagnostically. Clinical signs were limited to the 3 pigs that were exposed oronasally and parenterally to virulent virus even though the dexamethasone-treated pigs shed more virus for much longer than did those exposed directly to virus.

Animals↗