Photo of Penghua  Wang, Ph.D

Penghua Wang, Ph.D

Assistant Professor
Academic Office Location:
Department of Immunology
UConn Health
263 Farmington Avenue
Room L3057
Farmington, CT 06030-1319
Phone: 860-679-6393
860-679-6396
Fax: 860-679-1868
Email: pewang@uchc.edu
Curriculum Vitae:
Education
DegreeInstitutionMajor
B.Sc.Sun Yat-sen UniversityBiochemistry
Ph.D.The National University of SingaporeBiochemistry

Post-Graduate Training
TrainingInstitutionSpecialty
PostdoctoralYale UniversityPostdoctoral Associate

Awards
Name of Award/HonorAwarding Organization
Career Development AwardNortheast Biodefense Center, NIAID

Immunobiology II, MEDS 5330

Name & DescriptionCategoryRoleTypeScopeStart YearEnd Year
NIH VIRB Study SectionStudy SectionAd hoc memberExternalNational2018
VirusesEditorial BoardGuest EditorExternalInternational20182019
Antimicrobial Agents and ChemotherapyProfessional/Scientific JournalReviewing EditorExternalInternational20172020
NIH, Non-HIV Infectious Agent Detection/Diagnostics, Food Safety, Sterilization/Disinfection and Bioremediation Special Emphasis PanelStudy SectionAd hoc memberExternalNational2016
American Society For VirologyProfessional/Scientific OrganizationRegular MemberExternalNational2015
Frontiers in Cellular and Infection Microbiology, Frontiers in VirologyProfessional/Scientific JournalAssociate EditorExternalInternational2015

My laboratory is  interested in host-virus interactions, with a focus on RNA viruses in vivo and in vitro. Specifically, we attempt to understand pathogenic mechanisms of viral infection at the cellular and animal levels, and study the molecular function of host genes that influence viral pathogenesis and the disease outcomes. On the host end, we are keen on the innate immune system, detection of viruses and initiation of innate antiviral immune responses.  On the viral end, we hope to understand the mechanisms of immune evasion and modulation of cellular functions by viral proteins. 

My laboratory now has seevral active projects. 


1.  The physiological function of UBXNs in antiviral immunity. The human genome encodes 13 UBXNs containing a conserved UBX domain, which shares weak homology with ubiquitin at the protein level but adopts the same three dimensional fold as ubiquitin. It has been recently shown that several UBXN proteins bind to a large number of E3 ubiquitin ligases, suggesting that the UBXN proteins participate in global regulation of protein turnover, most likely including immune proteins. However, the molecular function of the majority of UBXN proteins is largely unknown. We  characterized UBXN1 as a negative regulator of a major antiviral immune signaling pathway-RLR in cell culture. We are now generating Ubxn1 conditional knockout mouse and will characterize it in viral and inflammatory disease models. More recently we  found that UBXN3B positively regulates STING-dependent innate immune responses in mice. Next we will address the role of UBXN3B adaptive immune response to viral infection. We have also recently shown that UBXN3B restricts RNA virus infection in mice and interestingly Chikungunya arthritis pathogenesis. We will elucidate the underlying mechanism and extend to collagen induced arthritis (mouse model of rheumatoid arthritis). 


2. Molecular mechanisms of viral infection-induced placentation defectsLarge-scale phenotyping efforts have demonstrated that approximately 25–30% of essentail mouse gene knockouts cause intrauterine lethality. 68% causes placental defects. Placentation defects are highly prevalent in embryonic lethal mouse mutants.  Viral infections in pregnancy are major causes of maternal and fetal morbidity and mortality. Questions:  Does Zika virus infection during pregnancy alter expression and /or function of placentation genes?


3. The role of tripartite motif-containing proteins (TRIM) in type I IFN responses.  There are now more than 60 TRIM proteins, many of which are E3 ligases and regulators of innate immune signaling. Some directly interfere with viral life cycle. We are interested in investigating TRIM function in Zika virus replciation and JAK-STAT signaling.   


4. The molecular function of macrophage scavenger receptor 1 (MSR1) in viral infection.  MSR1 is a member of the scavenger receptor family (SR)  that is structurally very heterogeneous and is composed of members with little or no homology. MSR1 is believed to participate in TLR signaling. We recently found that MSR1 controls CHIKV infection and regulates autophagy. We will continue elucidating the underlying molecular mechanism. 

Open to incoming gradute students 2018 Fall and 2019 spring 

Journal Articles

Reviews

Title or AbstractTypeSponsor/EventDate/YearLocation
UBXNs, new players in antiviral immunityTalkDepartment of Virology, Mount Sinai School of Medicine2018New York City, NY
STING Controls Chikungunya Virus Infection and PathogenesisTalkShenzhen CDC, Tsinghua University2016Shenzhen, China
NOD Like Receptor 6: Not A Nod to Enteric VirusesTalkDepartment of Medicine, McGill University2016Montreal Canada
A critical role for STING in the control of Chikungunya virus pathogenesisPosterKeystone Symposium2016Austin, TX, USA