Immune response to intranasal and intraperitoneal immunization with Kaposi's sarcoma-associated herpesvirus in mice

Sakamoto, Kouta; Asanuma, Hideki; Nakamura, T.; Kuriyama, Takayuki; Sata, Tetsutaro; Katano, Harutaka

doi:10.1016/j.vaccine.2010.02.091

Cited by 6 publications

(4 citation statements)

References 42 publications

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“…We hypothesize that all these homologs have an important role in regulating gammaherpesvirus tropism through both positive and negative effects. Yes (in heterologous model) (44) No (14) (immunodominant protein -immunological decoy) (14) No (polyserum) (38) …”

Section: Discussionmentioning

confidence: 99%

The Bovine Herpesvirus 4 Bo10 Gene Encodes a Nonessential Viral Envelope Protein That Regulates Viral Tropism through both Positive and Negative Effects

Machiels¹,

Lété²,

Fays³

et al. 2011

J Virol

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All gammaherpesviruses encode a glycoprotein positionally homologous to the Epstein-Barr virus gp350 and the Kaposi's sarcoma-associated herpesvirus (KSHV) K8.1. In this study, we characterized the positional homologous glycoprotein of bovine herpesvirus 4 (BoHV-4), encoded by the Bo10 gene. We identified a 180-kDa gene product, gp180, that was incorporated into the virion envelope. A Bo10 deletion virus was viable but showed a growth deficit associated with reduced binding to epithelial cells. This seemed to reflect an interaction of gp180 with glycosaminoglycans (GAGs), since compared to the wild-type virus, the Bo10 mutant virus was both less infectious for GAG-positive (GAG ؉ ) cells and more infectious for GAG-negative (GAG ؊ ) cells. However, we could not identify a direct interaction between gp180 and GAGs, implying that any direct interaction must be of low affinity. This function of gp180 was very similar to that previously identified for the murid herpesvirus 4 gp150 and also to that of the Epstein-Barr virus gp350 that promotes CD21؉ cell infection and inhibits CD21 ؊ cell infection. We propose that such proteins generally regulate virion attachment both by binding to cells and by covering another receptor-binding protein until they are displaced. Thus, they regulate viral tropism both positively and negatively depending upon the presence or absence of their receptor.Many viruses use a single glycoprotein for both cell binding and membrane fusion. Herpesviruses are more complex. Three proteins-gB, gH, and gL-form a core fusion machinery conserved in the Alpha-, Beta-, and Gammaherpesvirinae subfamilies (21). Most herpesviruses also encode at least one additional receptor-binding protein that is more specific for a given virus subfamily. For example, herpes simplex virus first attaches to cells by gB or gC binding to the heparan sulfate moieties of the cell surface proteoglycans. gD must then bind for fusion to occur (47).Our understanding of gammaherpesvirus glycoprotein functions is more limited. This is due to the fact that the human gammaherpesviruses Epstein-Barr virus (EBV) and Kaposi's sarcoma-associated herpesvirus (KSHV) show limited lytic growth in vitro. Nevertheless, understanding how viral glycoproteins function is important for vaccination and for the development of neutralizing antibodies. While gB, gH, and gL are probably the key partners of the gammaherpesvirus membrane fusion machinery (22,39,41), the function of accessory entry proteins is less clear. EBV gp350/220 is a highly glycosylated membrane protein that adopts its 2 differently sized forms by alternative splicing (23). It is the most abundant protein in the virion envelope, binds to complement receptor 2 (CD21) on B cells (40,49), and is a target for antibodies that neutralize B cell infection (53). Soluble recombinant gp350 can also inhibit EBV infection of CD21-positive (CD21 ϩ

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Section: Discussionmentioning

confidence: 99%

The Bovine Herpesvirus 4 Bo10 Gene Encodes a Nonessential Viral Envelope Protein That Regulates Viral Tropism through both Positive and Negative Effects

Machiels¹,

Lété²,

Fays³

et al. 2011

J Virol

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“…The route of vaccine administration is an important factor for vaccination efficiency (15,16). The kinetics of the attenuated DPV vaccine strain CHa determined that subcutaneous administration had a larger effect on the vaccine virus distribution in tissue than the oral and nasal routes of administration did (17).…”

mentioning

confidence: 99%

An Attenuated Duck Plague Virus (DPV) Vaccine Induces both Systemic and Mucosal Immune Responses To Protect Ducks against Virulent DPV Infection

Huang

Jia

Wang

et al. 2014

Clin Vaccine Immunol

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c Duck plague (DP) is a severe disease caused by DP virus (DPV). Control of the disease is recognized as one of the biggest challenges in avian medicine. Vaccination is an efficient way to control DPV, and an attenuated vaccine is the main routine vaccine. The attenuated DPV vaccine strain CHa is a modified live vaccine, but the systemic and mucosal immune responses induced by this vaccine have been poorly understood. In this study, the immunogenicity and efficacy of the vaccine were evaluated after subcutaneous immunization of ducks. CD4؉ and CD8 ؉ T cells were counted by flow cytometry, and humoral and mucosal Ig antibodies were analyzed by enzyme-linked immunosorbent assay (ELISA). The results showed that high levels of T cells and Ig antibodies were present postimmunization and that there were more CD4 ؉ T cells than CD8 ؉ T cells. Titers of humoral IgG were higher than those of humoral IgA. Local IgA was found in each sample, whereas local IgG was found only in the spleen, thymus, bursa of Fabricius, harderian gland, liver, bile, and lung. In a protection assay, the attenuated DPV vaccine completely protected ducks against 1,000 50% lethal doses (LD 50 ) of the lethal DPV strain CHv via oral infection. These data suggest that this subcutaneous vaccine elicits sufficient systemic and mucosal immune responses against lethal DPV challenge to be protective in ducks. This study provides broad insights into understanding the immune responses to the attenuated DPV vaccine strain CHa through subcutaneous immunization in ducks.

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“…Vaccinating with KSHV-encoded proteins may produce antibodies to neutralize KSHV virus in animal experiments [50]. As KSHV infection is common in African countries and remains a major cause of morbidity and mortality in HIV-infected patients, moreover, there is no definite cure therapies, developing new approaches for treatment KSHV is needed.…”

Section: Kaposi’s Sarcoma-associated Herpesvirusmentioning

confidence: 99%

Activation and counteraction of antiviral innate immunity by KSHV: an update

Wei

Lan

2018

Science Bulletin

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The innate immune responses triggering production of type I interferons and inflammatory cytokines constitute a nonspecific innate resistance that eliminates invading pathogens including viruses. The activation of innate immune signaling through pattern recognition receptors (PRRs) is by sensing pathogen-associated molecular patterns derived from viruses. According to their distribution within cells, PRRs are classified into three types of receptors: membrane, cytoplasmic, and nuclear. Kaposi’s sarcoma-associated herpesvirus (KSHV), a large DNA virus, replicates in the nucleus. Its genome is protected by capsid proteins during transport in the cytosol. Multiple PRRs are involved in KSHV recognition. To successfully establish latent infection, KSHV has evolved to manipulate different aspects of the host antiviral innate immune responses. This review presents recent advances in our understanding about the activation of the innate immune signaling in response to infection of KSHV. It also reviews the evasion strategies used by KSHV to subvert host innate immune detection for establishing a persistent infection.

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Immune response to intranasal and intraperitoneal immunization with Kaposi's sarcoma-associated herpesvirus in mice

Cited by 6 publications

References 42 publications

The Bovine Herpesvirus 4 Bo10 Gene Encodes a Nonessential Viral Envelope Protein That Regulates Viral Tropism through both Positive and Negative Effects

The Bovine Herpesvirus 4 Bo10 Gene Encodes a Nonessential Viral Envelope Protein That Regulates Viral Tropism through both Positive and Negative Effects

An Attenuated Duck Plague Virus (DPV) Vaccine Induces both Systemic and Mucosal Immune Responses To Protect Ducks against Virulent DPV Infection

Activation and counteraction of antiviral innate immunity by KSHV: an update

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