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PubMed1978

Interactions between effector cell activity and lymphokines: implications for recovery from herpesvirus infections.

The destruction of herpesvirus-infected target cells by antibody-dependent and direct cell cytotoxicity was enhanced by the presence of bovine lymphokine-containing preparations. To relate these effects to possible in vivo mechanisms of recovery, several in vitro approaches were used to measure the effects of lymphokine-containing preparations on controlling viral spread. In the first approach it was shown that in the presence of lymphokines, virus-infected cells could be killed earlier in the replication cycle by the mechanism of antibody-dependent cell cytotoxicity, thus possibly limiting spread of virus. That this was indeed the case was demonstrated by a decrease in the area of viral-induced cytopathology as well as in the total number of infected cells present. Secondly, the amount of infectious virus released was also markedly reduced in cultures incubated with lymphokines and immune peripheral blood lymphocytes as compared to cultures treated with either component alone. Finally, lymphokines caused the activation of macrophages. These results are discussed in terms of how various immune parameters may interact in a positive way so as to aid in the recovery from virus infection.

Antibody-Dependent Cell Cytotoxicity↗
PubMed2001

Vaccination against murine gamma-herpesvirus infection.

The gamma-herpesviruses establish life-long latency in the host and are important human pathogens. T cells play a major role in controlling the initial acute infection and subsequently maintaining the virus in a quiescent state. However, the nature of the T-cell response to gamma-herpesvirus infection and the requirements for effective vaccination are poorly understood. The recent development of a murine gamma-herpesvirus (murine herpesvirus-68 [MHV-68]) has made it possible to analyze T-cell responses and test vaccination strategies in a small animal model. Intranasal infection with MHV-68 induces an acute infection in the lung and the subsequent establishment of long-term latency, which is associated with splenomegaly and an infectious mononucleosis-like syndrome. Here we review the T-cell response to different phases of the infection and the impact of vaccination against either lytic-cycle, or latency-associated T-cell epitopes.

Animals↗
PubMed1986

Herpesvirus infection prevents activation of cytoplasmic cholesteryl esterase in arterial smooth muscle cells.

Herpesvirus infection has been shown to alter the cholesteryl ester cycle in avian arterial smooth muscle cells, resulting in cytoplasmic cholesteryl ester accumulation (Hajjar, D. P., Falcone, D. J., Fabricant, C. G., and Fabricant, J. (1985) J. Biol. Chem. 260, 6124-6128). In this study, we attempted to define some of the regulatory mechanisms associated with the control of cytoplasmic cholesteryl esterase in Marek's disease herpesvirus (MDV)-infected cells. We found that cholesteryl esterase activity in MDV-infected cells could not be activated by dibutyryl cyclic AMP, dibutyryl cyclic AMP added together with protein kinase, or agonists of adenylate cyclase. Activation of cytoplasmic cholesteryl esterase activity occurred in uninfected cells and in cells infected with a control virus, turkey herpesvirus. Furthermore, the rate of cholesterol efflux from arterial smooth muscle cells challenged with dibutyryl cyclic AMP was unchanged in MDV-infected cells as compared to uninfected or turkey herpesvirus-infected cells in which efflux was increased. We propose that the reduced cytoplasmic cholesteryl esterase activity in lipid-laden, herpesvirus-infected cells is due partly to its inability to be activated by the cyclic AMP-protein kinase mechanism. This may contribute to the pathologic changes seen in MDV-infected arterial cells, including accumulation of intracellular cholesteryl esters.

Animals↗
PubMed1988

Herpesvirus infections (cytomegalovirus, herpes simplex virus, varicella-zoster virus). How to use ganciclovir (DHPG) and acyclovir.

Herpes viruses (HSV, CMV, VZ) are very frequent in AIDS patients and often exist in a chronic or progressive form. Clinically evident CMV retinitis occurs in approximately 10 per cent of AIDS patients but can be effectively treated with a new nucleoside analogue DHPG (Gancyclovir). Perianal ulcers, proctitis, and other clinical syndromes caused by HSV can be effectively treated with acyclovir (ACV) and HSV recurrences can be prevented by daily administration of ACV. Zoster in a young adult may be the first indication of immunodeficiency due to HIV. Because VZV is less susceptible to ACV than HSV, intravenous ACV or high-dose oral therapy is required to achieve inhibitory blood levels.

Acquired Immunodeficiency Syndrome↗
PubMedDate not supplied

Gallid-1 herpesvirus infection in the chicken. 3. Reinvestigation of the pathogenesis of infectious laryngotracheitis in acute and early post-acute respiratory disease.

Specific-pathogen-free chickens were infected via the trachea when 4 weeks old with 2000 plaque-forming units (PFU) of the virulent Australian infectious laryngotracheitis (ILT) virus strain CSW-1. Titers of ILT virus in the trachea were greatest (10(7.0) PFU/ml in washings, 10(6.0) PFU/g of tissue) 2-4 days postinfection (PI). Infectivity then declined rapidly, to become undetectable by 7 days PI, although highly localized areas of ILT antigen in the tracheal epithelium were occasionally observed by fluorescent antibody staining at 7 and 8 days PI. Tracheal organ cultures established 7 and 8 days PI provided no evidence of latent ILT virus infection at this immediate post-acute stage of pathogenesis. ILT virus was not isolated from peripheral blood leukocytes or lymphoid organs (spleen, bursa, thymus). ILT virus was found in the trigeminal ganglia and/or brain in 14 of 36 chickens (40%) examined between 4 and 7 days after intratracheal inoculation, but it was not in these tissues in five chickens examined at 8 days PI. Virus was also detected at 6 days PI in the trigeminal ganglia in one of five chickens infected by the conjunctival route. These data indicate that the early pathogenesis of ILT (CSW-1) infection frequently involves the tissues of the nervous system. In acute ILT in 4-week-old chickens, interferon-alpha/beta activity was not detectable in serum or tracheal exudates within 14 days PI, but tracheal washings contained significant virus-neutralizing activity by 7 and 8 days PI. In 3-day-old chickens infected via the trachea with 200 PFU of ILT CSW-1, the clearance of ILT virus from the trachea was similar to that observed in 4-week-old chickens, but ILT virus spread systemically to the livers of 20% by 5-7 days PI.

Animals↗
PubMed1976

Antibody-dependent cell-mediated cytotoxicity in cows: comparison of effector cell activity against heterologous erthrocyte and herpesvirus-infected bovine target cells.

Bovine peripheral blood leukocytes (PBL) and cells collected from the bovine mammary gland were assayed for antibody-dependent cell-mediated cytotoxicity (ADCC) against chicken erythrocyte (CRBC) and bovine herpesvirus-infected bovine kidney cell targets. Bovine antisera were used to sensitize target cells. Both PBL and mammary leukocytes expressed ADCC, with the latter cell population having greater activity against both target cells. Only the CRBC target cells were killed by nonadherent PBL and phagocyte-depleted PBL. Nonadherent mammary leukocytes, rich in monocytes and macrophages, did kill virus-infected target cells. Carbonyl iron-treated mammary leukocytes failed to kill virus-infected targets but could destroy CRBC targets. Antimacrophage serum inhibited lysis of both CRBC and virus-infected targets, but antilymphocyte serum only inhibited CRBC killing. These observations indicated that at least two kinds of cells could mediate ADCC against CRBC but only cells of the mononuclear phagocytic series could kill virus-infected target cells. The herpesvirus-infected target cells became susceptible to ADCC 9 h after virus infection. A case is made for investigating the phenomenon of ADCC using in vitro systems that closely mimic the in vivo situation. The possible role of the ADCC mechanism as instrumental in causing recovery from herpesvirus infections is discussed.

Animals↗
PubMed1976

An experimental model for disseminated herpesvirus infection of the neonate.

Pregnant mice at 10 days of gestation were more susceptible to vaginal inoculation with herpesvirus, type 2, than were nonpregnant mice. This mouse model system also was used to compare delivery through a birth canal contaminated with herpesvirus, type 2, to delivery after maternal paranteral inoculation by the same virus. Approximately 26 per cent of newborn mice either died or had evidence of disseminated herpesvirus infections after delivering through a vagina inoculated with herpesvirus, whereas only 4 per cent of newborn mice died after subcutaneous inoculation of pregnant animals. Only 1 per cent of neonates delivered of subcutaneously inoculated pregnant mice had any evidence of herpesvirus infection. Pregnant mice immunized to herpesvirus, type 1, had significantly less newborn infection after delivery through a herpesvirus-inoculated birth canal when compared to nonimmunized mice.

Animals↗
PubMed2002

Critical role of complement and viral evasion of complement in acute, persistent, and latent gamma-herpesvirus infection.

Several gamma-herpesviruses encode homologs of host regulators of complement activation (RCA) proteins, suggesting that they have evolved immune evasion strategies targeting complement. We evaluated the role of complement factor C3 (C3) and the murine gamma-herpesvirus 68 (gammaHV68) RCA protein in viral pathogenesis. Deletion of the gammaHV68 RCA protein decreased virulence during acute CNS infection, and this attenuation was specifically reversed by deletion of host C3. The gammaHV68 RCA protein was also important for persistent viral replication and virulence in IFNgammaR(-/-) mice. In addition, C3 played a role in regulating latency, but this was not counteracted by the gammaHV68 RCA protein. We conclude that complement is a key host defense against gamma-herpesvirus infection and that gamma-herpesviruses have evolved an immune evasion strategy that is effective against complement-mediated antiviral responses during acute but not latent infection.

Acute Disease↗
PubMed1978

Mechanisms of recovery from Herpesvirus infections -a review.

A variety of specific immunological mechanisms have been shown to be effective at neutralizing herpesviruses or destroying herpesvirus infected cells. These include both humoral and cell mediated immune responses or combinations thereof. Thus, it is genarlly accepted that humoral immunity is probably responsible for preventing reinfection whereas cellular immunity, mediated by T lymphocytes or by the interaction of antibody and Fc receptor bearing cells, is more important in recovery from infections. In addition to these specific responses to herpesvirus infection, a number of nonspecific cellular and humoral components have been shown to inhibit the progression of virus replication and therefore, have been implicated in assisting the host in the recovery process. The various interactions and counteractions between the various nonspecific and specific components of the immune response are discussed with respect to their role in recovery from both primary and recurrent disease as well as how they may eventually be manipulated so as to control herpesvirus recrudescent disease.

Animals↗
PubMed1983

Association of herpesvirus infections with T-lymphocyte-subset alterations, glomerulopathy, and opportunistic infections after renal transplantation.

We studied the interrelation among herpes-virus infections, T-lymphocyte subsets, opportunistic infections, and renal histopathology in 28 recipients of renal allografts. All primary or reactivated herpesvirus infections occurring in the first three months after transplantation in recipients of cadaveric grafts accompanied persistent inversions in the ratio of OKT4 (helper/inducer) to OKT8 (cytotoxic/suppressor) lymphocytes. In the less heavily immunosuppressed recipients of organs of living related donors, these inversions were seen only in association with clinically apparent cytomegalovirus infections. Five of seven opportunistic infections occurred in patients with OKT4/OKT8 ratios of less than 1.0. Biopsy specimens from patients with renal dysfunction occurring in association with a low OKT4/OKT8 ratio frequently revealed glomerular damage rather than acute cellular rejection. Monitoring of T-lymphocyte subsets provides early evidence of herpesvirus infections and identifies patients at increased risk for opportunistic infection after renal transplantation.

Biopsy↗
PubMed1977

Epstein-Barr herpesvirus infection: inhibition by immunologically induced mediators with interferon-like properties.

When sensitized leukocytes were re-exposed to EBV antigen or to tuberculin-purified protein derivatives, they produced lymphokines, including the migration inhibition factor, which inhibited the migration of guinea-pig peritoneal exudate cells, and other lymphokines with the characteristics of interferon, which inhibited EBV-induced transformation and EBV superinfection of target cells. Unsensitized leucocytes from sero-negative adults and from neonates did not produce lymphokines when challenged with the antigens. This indicates that cell-mediated immunity and its associated soluble mediators may be involved in the control of EBV infection and that the interferon release assay is a useful in vitro correlate for the study of cellular immunity to EBV.

Antibodies, Viral↗
PubMed2006

Equine herpesvirus 1 glycoprotein D expressed in E. coli provides partial protection against equine herpesvirus infection in mice and elicits virus-neutralizing antibodies in the horse.

The envelope glycoprotein D of EHV-1 (EHV-1 gD) is essential for virus infectivity and entry of virus into cells and is a potent inducer of virus-neutralizing antibody. In this study, truncated EHV-1 gD (gDt) was expressed with a C-terminal hexahistidine tag in E. coli using a pET vector. Western blot analysis using an anti-gD monoclonal antibody demonstrated the presence of gDt bands at 37.5, 36, 29.5 and 28 kDa. The immunogenicity and protective efficacy of partially purified gDt was compared with gD expressed in insect cells by a recombinant baculovirus (Bac gD) using a BALB/c mouse model of EHV-1 respiratory infection. The proteins were also compared in a prime-boost protocol following an initial inoculation with gD DNA. gDt elicited similar levels of gD-specific antibody and neutralizing antibody compared with Bac gD and also provided a similar level of protection against EHV-1 challenge in mice. Inoculation of horses with gDt elicited EHV-1 gD-specific antibodies including virus-neutralizing antibody, suggesting that despite the lack of glycosylation, E. coli may be a useful vehicle for large scale production of EHV-1 gD for vaccine studies.

Animals↗
PubMed1975

Epidemiological studies of Epstein-Barr herpesvirus infection in Western Australia.

In a study of a Caucasian population in Western Australia the prevalence of antibodies to Epstein-Barr virus (EBV) was 41% in the 9- to 10-year age group, 80% in the 16 to 19-year age group and 92% in young adults. The age-specific annual seroconversion rates indicated two peaks of primary EBV infection in the population studied - one under 5 years of age and the other at adolescence. The geometric mean titre rose with age, from 23 at 5-6 years to 53 at 36-40 years. It was shown that in 73 families studied there was evidence of probable spread of EBV infection among siblings, particularly between those of the same sex. Serological study of patients with infectious mononucleosis indicated that 100% of those examined had antibody to EBV and the geometric mean titre was elevated to 210. Rising titres and seroconversion was demonstrated in these patients together with successful establishment of EBV-carrying cell lines from the peripheral blood in two-thirds of the cases.

Adolescent↗