Murid herpesvirus-4 lacking thymidine kinase reveals route-dependent requirements for host colonization
| Autor: | Debbie E. Wright, Philip G. Stevenson, Michael Gill, Christopher M. Smith, Janet S. May |
|---|---|
| Jazyk: | angličtina |
| Rok vydání: | 2009 |
| Předmět: |
Rhadinovirus
Population Respiratory System medicine.disease_cause Thymidine Kinase Herpesviridae Virus 03 medical and health sciences Gene Knockout Techniques Mice Viral Proteins 0302 clinical medicine Peritoneum Virology medicine Animals education Lung 030304 developmental biology 0303 health sciences education.field_of_study Mice Inbred BALB C biology Animal Murid herpesvirus 4 Herpesviridae Infections biology.organism_classification 3. Good health Tumor Virus Infections medicine.anatomical_structure Lytic cycle Thymidine kinase 030220 oncology & carcinogenesis Female |
| Zdroj: | The Journal of General Virology |
| ISSN: | 1465-2099 0022-1317 |
| Popis: | Gammaherpesviruses infect at least 90 % of the world's population. Infection control is difficult, in part because some fundamental features of host colonization remain unknown, for example whether normal latency establishment requires viral lytic functions. Since human gammaherpesviruses have narrow species tropisms, answering such questions requires animal models. Murid herpesvirus-4 (MuHV-4) provides one of the most tractable. MuHV-4 genomes delivered to the lung or peritoneum persist without lytic replication. However, they fail to disseminate systemically, suggesting that the outcome is inoculation route-dependent. After upper respiratory tract inoculation, MuHV-4 infects mice without involving the lungs or peritoneum. We examined whether host entry by this less invasive route requires the viral thymidine kinase (TK), a gene classically essential for lytic replication in terminally differentiated cells. MuHV-4 TK knockouts delivered to the lung or peritoneum were attenuated but still reached lymphoid tissue. In contrast, TK knockouts delivered to the upper respiratory tract largely failed to establish a detectable infection. Therefore TK, and by implication lytic replication, is required for MuHV-4 to establish a significant infection by a non-invasive route. |
| Databáze: | OpenAIRE |
| Externí odkaz: |
|