Ultrastructural Changes of the Tracheal Epithelium after Vaccination of Day-Old Chickens with the La Sota Strain of Newcastle Disease Virus

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130

144

Section: Cells and Viruses C Carpio Brain (Ccb) Cellsmentioning

confidence: 99%

The Major Portal of Entry of Koi Herpesvirus in Cyprinus carpio Is the Skin

Costes

Raj

Michel

et al. 2009

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130

144

“…The cells were then scraped off and prepared for electron microscopy. Epon blocks and sections were prepared as described previously (49). Sections were analyzed by using a Tecnai Spirit transmission electron microscope (FEI, Eindhoven, The Netherlands), and electron micrographs were taken by using a bottom-mounted 4K-by-4K-resolution Eagle camera (FEI).…”

Section: Animalsmentioning

confidence: 99%

The Major Envelope Glycoprotein of Murid Herpesvirus 4 Promotes Sexual Transmission

Zeippen

Javaux

Xiao

et al. 2017

Gammaherpesviruses are important human and animal pathogens. Infection control has proven difficult because the key process of transmission is ill understood. Murid herpesvirus 4 (MuHV-4), a gammaherpesvirus of mice, is transmitted sexually. We show that this depends on the major virion envelope glycoprotein gp150. gp150 is redundant for host entry, and in vitro, it regulates rather than promotes cell binding. We show that gp150-deficient MuHV-4 reaches and replicates normally in the female genital tract after nasal infection but is poorly released from vaginal epithelial cells and fails to pass from the female to the male genital tract during sexual contact. Thus, we show that the regulation of virion binding is a key component of spontaneous gammaherpesvirus transmission.IMPORTANCE Gammaherpesviruses are responsible for many important diseases in both animals and humans. Some important aspects of their life cycle are still poorly understood. Key among these is viral transmission. Here we show that the major envelope glycoprotein of murid herpesvirus 4 functions not in entry or dissemination but in virion release to allow sexual transmission to new hosts. KEYWORDS gammaherpesvirus, glycoprotein, release, transmission T ransmission is the main motor of viral evolution, and the large disease burden imposed by human gammaherpesviruses reflects very high infection prevalences due to efficient transmission from carriers to new hosts (1). Epstein-Barr virus (EBV) and Kaposi's sarcoma-associated herpesvirus (KSHV) infect up to 90% (2) and 30% (3) of humans worldwide, respectively. Endemic infections are maintained chiefly by carriers shedding virus in their saliva. However, in populations with a low prevalence of infection, sexual transmission becomes important due to increased contact (4). This was seen clearly for KSHV transmission associated with HIV infection (5) and may also apply to EBV (6).While interrupting transmission is the sine qua non of infection control, analyzing EBV and KSHV transmission has proven difficult. Natural EBV infection is asymptomatic for at least a month (6), and experimental transmission is made difficult by many EBV and KSHV functions being host specific. However, gammaherpesviruses colonize most mammals, so related animal viruses, such as murid gammaherpesvirus 4 (MuHV-4), provide another way to understand infection in vivo (7). Luciferase (Luc) imaging of MuHV-4 infection (8) revealed genital infection following intranasal (i.n.) inoculation of female mice, which then spread to naive males by sexual contact (9). This has provided

“…The cells were then scraped off and prepared for electron microscopy. Epon blocks and sections were prepared as described elsewhere (36). Sections were analyzed using a Technai Spirit transmission electron microscope (FEI, Eindhoven, The Netherlands), and electron micrographs were taken using a bottom-mounted 4-by-4 K Eagle camera (FEI).…”

Section: Cells and Viruses Bhk-21mentioning

confidence: 99%

Deletion of Murid Herpesvirus 4 ORF63 Affects the Trafficking of Incoming Capsids toward the Nucleus

Latif

Machiels

Xiao

et al. 2016

Gammaherpesviruses are important human and animal pathogens. Despite the fact that they display the classical architecture of herpesviruses, the function of most of their structural proteins is still poorly defined. This is especially true for tegument proteins. Interestingly, a potential role in immune evasion has recently been proposed for the tegument protein encoded by Kaposi's sarcoma-associated herpesvirus open reading frame 63 (ORF63). To gain insight about the roles of ORF63 in the life cycle of a gammaherpesvirus, we generated null mutations in the ORF63 gene of murid herpesvirus 4 (MuHV-4). We showed that disruption of ORF63 was associated with a severe MuHV-4 growth deficit both in vitro and in vivo. The latter deficit was mainly associated with a defect of replication in the lung but did not affect the establishment of latency in the spleen. From a functional point of view, inhibition of caspase-1 or the inflammasome did not restore the growth of the ORF63-deficient mutant, suggesting that the observed deficit was not associated with the immune evasion mechanism identified previously. Moreover, this growth deficit was also not associated with a defect in virion egress from the infected cells. In contrast, it appeared that MuHV-4 ORF63-deficient mutants failed to address most of their capsids to the nucleus during entry into the host cell, suggesting that ORF63 plays a role in capsid movement. In the future, ORF63 could therefore be considered a target to block gammaherpesvirus infection at a very early stage of the infection. IMPORTANCEThe important diseases caused by gammaherpesviruses in human and animal populations justify a better understanding of their life cycle. In particular, the role of most of their tegument proteins is still largely unknown. In this study, we used murid herpesvirus 4, a gammaherpesvirus infecting mice, to decipher the role of the protein encoded by the viral ORF63 gene. We showed that the absence of this protein is associated with a severe growth deficit both in vitro and in vivo that was mainly due to impaired migration of viral capsids toward the nucleus during entry. Together, our results provide new insights about the life cycle of gammaherpesviruses and could allow the development of new antiviral strategies aimed at blocking gammaherpesvirus infection at the very early stages. G ammaherpesviruses (␥HVs) are widespread viruses that cause lifelong infections in many mammalian species (1) and represent a significant cause of diseases (2, 3). Epstein-Barr virus (EBV; genus Lymphocryptovirus) and Kaposi's sarcoma-associated herpesvirus (KSHV; genus Rhadinovirus genus) are highly prevalent in human populations (3, 4) and are associated with several cancers (5). Despite the burden associated with these infections in some regions of the world, there is still no standard treatment (6). A better understanding of their biological cycle is therefore needed to develop new prophylactic or therapeutic strategies. As EBV and KSHV replicate poorly in vitro and have no establi...