ISSN: 2476-2024

Diagnostic Pathology: Open Access
Open Access

Our Group organises 3000+ Global Conferenceseries Events every year across USA, Europe & Asia with support from 1000 more scientific Societies and Publishes 700+ Open Access Journals which contains over 50000 eminent personalities, reputed scientists as editorial board members.

Open Access Journals gaining more Readers and Citations
700 Journals and 15,000,000 Readers Each Journal is getting 25,000+ Readers

This Readership is 10 times more when compared to other Subscription Journals (Source: Google Analytics)
  • Mini Review   
  • Diagn Pathol Open 2016, Vol 2(1): 124
  • DOI: 10.4172/2476-2024.1000124

Highly Neurovirulent Viruses Invade and Spread in the Brain Using the Host Reactions Triggered by Infection

Rihito Watanabe* and Masatoshi Kakizaki
Department of Bioinformatics, Faculty of Engineering, Soka University, Tokyo, Japan
*Corresponding Author : Rihito Watanabe, Department of Bioinformatics, Faculty of Engineering, Soka University, 1-236 Tangi-chou, Hachioji, Tokyo 192-8577, Japan, Tel: +81-426-91-9465, Email: rihitow@soka.ac.jp

Received Date: Feb 27, 2017 / Accepted Date: Mar 10, 2017 / Published Date: Mar 19, 2017

Abstract

Coronaviruses (CoVs) have relatively high mutation and RNA recombination rates and undergo rapid crossspecies transmission events in vitro and in vivo. The viruses have evolved diverse strategies to evade, blocking host immune responses, and resulting in an emergence of highly virulent CoVs to cause fatal diseases in human, such as severe acute respiratory syndrome (SARS) and Middle East respiratory syndrome (MERS). Among CoVs used for experimental studies, the cl-2 virus (cl-2), isolated from a neuropathogenic JHM viral strain (JHMV) of mouse hepatitis virus (MHV), shows extremely high virulence. All mice infected with cl-2 die within 3 days post-inoculation (dpi). Less virulent but still highly neurovirulent mutant viruses, soluble receptor resistant mutant virus (srr7) and Mu-3 virus (Mu-3), have been isolated from cl-2 and srr7, respectively. Although these viruses cause different pictures of neuropathologies with different distribution of viral antigens after infection, they use the same pathway to enter the brain before inducing lesions in the brain parenchyma. The pathway is formed as an astrocytic reticular network (ARN) after infection. The ARN functions as a conduit system in a similar way to a fibroblastic reticular network (FRN) in lymphoid organs. In addition, the viruses induce an immunosuppressive state in infected mice, mimicking endotoxin tolerance (ET), or lipopolysaccharide (LPS) tolerance. The immunosuppressive states are detected by; 1) pathological findings as 1a); a very low -level inflammatory response, 1b); the shrunken spleen, 1c); the refractory state to LPS challenge, and 1d); the local production of anti-inflammatory cytokines by neurons, and by 2) immunological studies, which showed 2a); the systemic production of anti-inflammatory cytokines by eliciting CD11b+Gra-1+ suppressor monocytes/macrophages (Mo/Mas).In addition, cultured splenic cells and Mo/Mas after infection exhibit 2b); low-level responses to stimulation of toll-like receptors (TLRs) 4 and 7, and 2c); the induction of Lewis X carbohydrate structure (Lex), which can trigger the C-type lectin-like receptor that initiates an immunosuppressive pathway, respectively.

Citation: Watanabe R, Kakizaki M (2017) Highly Neurovirulent Viruses Invade and Spread in the Brain Using the Host Reactions Triggered by Infection. Diagn Pathol Open 2: 124. Doi: 10.4172/2476-2024.1000124

Copyright: © 2017 Watanabe R, et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.

Top