The nightmare scenario that Reid envisions goes something like this: In
the next few years, an ambitious virologist uses widely-available
gene-editing technology to create a supervirus—a pathogen 10 times as
contagious as chicken pox and 10 times as deadly as the Ebola virus, but
with an incubation period of, say, 10 months. Based on that
programming, the entire world could be infected with the designer virus
before the first person even shows symptoms.
_______________
就是這篇文章了， 此文說這個製造病毒的項目是Zhengli-Li Shi， 也就是排名14， 倒數第二，而最後一名是通訊作者，也就是項目的真正主持人。 石小姐到底能起多大的作用？
A SARS-like cluster of circulating bat coronaviruses shows potential for human emergence
Vineet D Menachery,通訊作者， 第一作者
Boyd L Yount Jr,Kari Debbink,Sudhakar Agnihothram,Lisa E Gralinski,Jessica A Plante,Rachel L Graham,Trevor Scobey,
Xing-Yi Ge,湖南大學，做基因序列分析，沒有合成病毒紀錄
Eric F Donaldson,Scott H Randell,Antonio Lanzavecchia,Wayne A Marasco,
Zhengli-Li Shi 石正麗
Ralph S Baric 通訊作者
Nature Medicine
volume 21, pages1508–1513(2015)Cite this article
Vineet D. Menachery, PhD
Assistant Professor
Department of Microbiology & Immunology
Phone: (409) 266-6934
Mail Route: 0610
Office: Galveston National Laboratory (GNL) 5.200N
Lab: Keiller 2.144
Email: vimenach@utmb.edu
Web: themenacherylab.org
| Education |
|---|
Post-doctoral Fellowship
University of North Carolina at Chapel Hill | May 2017
Chapel Hill, NC |
PhD, Biological Sciences, concentration in Immunology
Washington University in Saint Louis | May 2010
St. Louis, MO |
BS, Microbiology, minor in Business Administration
Clemson University | May 2004
Clemson, SC |
| Research Interests |
|---|
| Coronaviruses, systems biology, aging, immunology, genetics, SARS-CoV, MERS-CoV, viral emergence |
| Current Research |
|---|
Utilizing
severe coronavirus infections, the Menachery Lab seeks to define
virus-host interactions that dictate disease outcomes taking advantage
of three cutting edge platforms: 1) reverse genetic systems for virus
generation, 2) a refined systems biology approach, and 3) diverse model
systems for infection. Described below, the current projects provide
insight into our approach and explore areas with implications for
understanding infection and disease.Examine
the dynamics of host-virus interactions within and between diverse
viral families. Employing uniform experimental platforms, these systems
based studies seek to identify common host pathways induced and/or
antagonized by various pathogenic viruses. The approach also leverages
differences between wild-type and mutant viruses to identify key
processes that drive pathogenic outcomes. The overall goal is to derive
mechanistic insight and develop novel avenues for antiviral treatment. Explore
the pathogenic and emergence potential of novel CoVs. The outbreaks of
both SARS and MERS-CoV underscore the need for continued surveillance of
zoonotic viruses. While CoV sequences have been identified, minimal
translational work has been undertaken. These studies evaluate the
likelihood of emergence, pathogenic potential, and efficacy of current
therapeutic platforms against existing coronavirus strains. Define
age dependent changes to host immunity via viral infection. Infectious
disease in the context of aging represents an opportunity to explore
changes to immunity as well as gain insights into a leading cause of
death among the elderly. Importantly, both SARS and MERS-CoV induce more
severe infection and increased mortality in aged human patients. This
phenotype is recapitulated in young and aged mouse models, allowing
exploration of host virus interaction that change as a product of aging.
These studies seek to identify, confirm, and validate changes in
pathway activation as well as develop treatments to mitigate disease in
the aged hosts. Examine the role of
host diversity in susceptibility to infection. In addition to aging,
host genetic diversity plays a critical role in the response to
respiratory virus infection. Employing the Collaborative Cross (CC), a
panel of recombinant inbred mice that captures genetic diversity similar
to the human population, we observe a wide spectrum of phenotypes.
These readouts can be dysregulated from each other, allowing fine
mapping to define specific genetic components that drive phenotypic
responses.
|
Ralph Baric, PhD
Professor
Department of Epidemiology
3304 MHRC, School of Public Health
919-966-3895
Research
Most of the research in our laboratory has used coronaviruses as
models to study the genetics of RNA virus transcription, replication,
persistence, and cross species transmission. We have also been using
alphavirus vaccine vectors to develop novel candidate vaccines against
caliciviruses. Specific areas of interest include:
1. Coronavirus Reverse Genetics and vaccine development.
We have developed infectious cDNAs from two coronaviruses. Specific
applications include: a) studying critical cis and trans acting factors
that regulate coronavirus subgenomic mRNA synthesis and replication, b)
rearranging the coronavirus gene order to study genome evolution and
function in coronavirus transcription and replication, c) identification
of the minimal coronavirus genome, d) development of coronavirus
replicon RNAs and coronavirus replicon particles for vaccine
development, e) expression of heterologous genes from coronavirus
vaccine vectors for swine and other important species.
2. Norwalk like virus (Calicivirus) vaccine development.
We are using the alphavirus, Venezuelan equine encephalitis virus
(VEE), as a vaccine vector for the Norwalk like viruses. Our research
encompasses: a) expression of Norwalk and SnowMountain virus capsid
proteins from VEE, b) biochemical and immunologic characterization of
these recombinant proteins, c) vaccine testing in mice, and d) use a
human challenge model to identify immunologic responses associated with
protection from NLV reinfection.
3. RNA virus transcription, replication and recombination.
Our laboratory has had a longstanding interest in using genetic
approaches to study coronavirus transcription, replication and RNA
recombination.
4. RNA virus persistence, cross species transmission and virus-host coevolution.
Our laboratory has studied the mechanism for coronavirus persistence
in vitro. This occurs by virus selection for resistant host cells that
down regulate the expression of the host receptor needed for coronavirus
docking and entry. The emergence of these resistant host cells
subsequently selects for the coevolution of virus variants that
recognize new receptors for docking and entry. Virus variants evolve
with expanded host range through recognition of phylogenetic homologues
of the normal coronavirus receptor. Consequently, we are studying the
mechanisms of RNA virus-host cell coevolution and virus receptor
interactions that regulate virus host range expansion.
Publications
Denison MR, Graham RL, Donaldson EF, Eckerle LD, Baric RS (2011).
Coronaviruses: an RNA proofreading machine regulates replication
fidelity and diversity. RNA Biol. 8(2):270-9.
——————————
石小姐的研究， 都是調查性質， 病毒採集回來鑑定一下DNA
Since
the 2002–2003 severe acute respiratory syndrome (SARS) outbreak
prompted a search for the natural reservoir of the SARS coronavirus,
numerous alpha- and betacoronaviruses have been discovered in bats
around the world. Bats are likely the natural reservoir of alpha- and
betacoronaviruses, and due to the rich diversity and global distribution
o...
