Varicella zoster virus glycoprotein C increases chemokine-mediated leukocyte migration

Varicella zoster virus (VZV) is a highly prevalent human pathogen that establishes latency in neurons of the peripheral nervous system. Primary infection causes varicella whereas reactivation results in zoster, which is often followed by chronic pain in adults. Following infection of epithelial cells in the respiratory tract, VZV spreads within the host by hijacking leukocytes, including T cells, in the tonsils and other regional lymph nodes, and modifying their activity. In spite of its importance in pathogenesis, the mechanism of dissemination remains poorly understood. Here we addressed the influence of VZV on leukocyte migration and found that the purified recombinant soluble ectodomain of VZV glycoprotein C (rSgC) binds chemokines with high affinity. Functional experiments show that VZV rSgC potentiates chemokine activity, enhancing the migration of monocyte and T cell lines and, most importantly, human tonsillar leukocytes at low chemokine concentrations. Binding and potentiation of chemokine activity occurs through the C-terminal part of gC ectodomain, containing predicted immunoglobulin-like domains. The mechanism of action of VZV rSgC requires interaction with the chemokine and signalling through the chemokine receptor. Finally, we show that VZV viral particles enhance chemokine-dependent T cell migration and that gC is partially required for this activity. We propose that VZV gC activity facilitates the recruitment and subsequent infection of leukocytes and thereby enhances VZV systemic dissemination in humans

Infectious laryngotracheitis: a review

Infectious laryngotracheitis (ILT) herpesvirus continues to cause outbreaks of respiratory disease in chickens world-wide. Sporadic cases of ILT occur in all classes of birds, including hobby/show/game chickens, broilers, heavy breeders, and commercial laying hens. These epornitics of ILT tend to occur where there are large populations of naïve, unvaccinated birds, i.e., in concentrated areas of broiler production. ILT virus can be transmitted through (a) chickens with acute upper respiratory tract disease, (b) latently infected "carrier" fowls, and (c) fomites and contaminated persons. Chicken flocks which are endemic infected with ILT virus occur only in some regions of countries or even in particular multiple-age production farms. In these cases modified live vaccines are actually used, even though these biological products, as well as wild ILTV strains, can establish latent infections. In the case of heavy breeders and laying hens, which are typically vaccinated against ILT, sporadic cases are often related to errors in vaccine application and to biosecurity failures

Human herpesvirus 8 (HHV-8) and the etiopathogenesis of Kaposi's sarcoma Herpesvírus humano tipo 8 (HHV-8) e a etiopatogênese do sarcoma de Kaposi

OBJECTIVE: To review the current literature on human herpesvirus 8 with particular attention to the aspects related to the etiopathogenesis of Kaposi's sarcoma. MATERIALS AND METHODS: The authors searched original research and review articles on specific aspects of human herpesvirus 8 infection, including virology, epidemiology, transmission, diagnosis, natural history, therapy, and Kaposi's sarcoma etiopathogenesis. The relevant material was evaluated and reviewed. RESULTS: Human herpesvirus 8 is a recently discovered DNA virus that is present throughout the world but with major geographic variation. In the Western world, the virus, transmitted mainly by means of sexual contact, is strongly associated with Kaposi's sarcoma and body cavity-based lymphoma and more controversially with multiple myeloma and other non-proliferative disorders. There is no specific effective treatment, but HIV protease inhibitors may play an indirect role in the clearance of human herpesvirus 8 DNA from peripheral blood mononuclear cells of HIV-infected patients. Human herpesvirus 8 DNA is present in saliva, but there are as yet no documented cases of nosocomial transmission to health care workers. The prevalence of human herpesvirus 8 among health care workers is probably similar to that in the general population. CONCLUSION: Human herpesvirus 8 appears to be, at least in Western Europe and United States, restricted to a population at risk of developing Kaposi's sarcoma. Human herpesvirus 8 certainly has the means to overcome cellular control and immune responses and thus predispose carriers to malignancy, particularly Kaposi's sarcoma. The wide diffusion of Human herpesvirus 8 in classic Kaposi's sarcoma areas appears to represent an important factor in the high incidence of the disease. However, additional co-factors are likely to play a role in the development of Kaposi's sarcoma.<br>OBJETIVO: O objetivo do presente artigo foi revisar a literatura recente em relação ao herpesvírus humano tipo 8, com ênfase especial aos aspectos relacionados à etiopatogênese do sarcoma de Kaposi. MÉTODOS: Os autores pesquisaram artigos de pesquisa original e revisões de literatura nos aspectos específicos da infecção pelo herpesvírus humano tipo 8, incluindo, virologia, epidemiologia, transmissão, diagnóstico, história natural e terapia. O material considerado relevante foi avaliado e revisado. RESULTADOS: O sarcoma de Kaposi é considerado ainda a malignidade mais comumente observada em pacientes infectados pelo HIV. Estudos epidemiológicos, assim como os baseados em técnicas de biologia molecular indicam que um agente sexualmente transmissível, independente do HIV, deve estar envolvido na etiologia do sarcoma de Kaposi, possivelmente como resultado da ação das cell signaling proteins superando os aspectos da resposta imune. O herpesvírus humano tipo 8 tem sido ainda sugerido como agente causal na patogênese de outras desordens, incluindo mieloma múltiplo, multicentric Castleman's disease, body cavity-based lymphoma, além de outras condições não-proliferativas como sarcoidose e pênfigo vulgar, embora grande parte dos estudos sorológicos apontem para uma soroprevalência em torno de 2 a 10%. O herpesvírus humano tipo 8 parece então, ser um vírus restrito a pessoas sob risco de desenvolver o sarcoma de Kaposi, associado à imunossupressão. O tratamento para o sarcoma de Kaposi é normalmente paliativo, e inclui a aplicação de vimblastina intra-lesional, crio-cirurgia, interferon-alpha e outras formas de terapia. Mais recentemente, os inibidores da protease, foram também sugeridos como possíveis agentes implicados na remissão do sarcoma de Kaposi associado ao HIV e no desaparecimento do herpesvírus humano tipo 8 das células mononucleares do sangue periférico. CONCLUSÃO: O herpesvírus humano tipo 8 está fortemente associado a todas as formas de sarcoma de Kaposi, multicentric Castleman's disease e body cavity-based lymphoma. Ainda, não existe tratamento definitivo para o sarcoma de Kaposi