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The Bouchard Lab Lab Members

Members of the Bouchard Lab in the Department of Biochemistry & Molecular Biology

Joseph Guarnieri

Bouchard Lab Member: Joseph Guarnieri

We hypothesize that HBx interaction with VDAC(s) is required for HBx localization to mitochondria and elevation of [Ca2+]mito and that this is linked to HBx elevation of [Ca2+]cyto and stimulation of HBV replication. Our goal is to determine whether HBx localization to mitochondria and elevation of [Ca2+]mito is required for HBx stimulation of HBV replication. To accomplish our goal, we will:

  1. Identify the amino acid(s) of HBx that mediate HBx localization to mitochondria and whether this localization requires an interaction with VDAC(s)
  2. Determine if HBx localization to mitochondria and/or interaction with VDAC(s) is required for HBx elevation of [Ca2+]mito and stimulation of HBV replication.

Our studies will be conducted in human hepatoblastoma HepG2 cells and cultured primary human hepatocytes. The results of the studies described here will define how HBx localizes to mitochondria and whether this localization and elevation of [Ca2+]mito stimulates HBV replication. The proposed studies are significant because they will address a gap in our knowledge of processes that regulate HBV replication and could identify novel drug targets for treating a chronic HBV infection.

Ronak Loonawat

Bouchard Lab Member: Ronak Loonawat

Hepatitis B virus (HBV) has come a long way from first being linked to "Australian Antigen" to now being one of the most dreadful viruses known to humans; chronically infecting 250 million people worldwide, HBV resulted in 887,000 deaths just in 2015 alone. Chronic HBV infection is a leading cause for hepatocellular carcinoma (HCC), which in turn is the second most prevalent cause of death related to cancer worldwide.

Mechanistically, the advancement from HBV infection to HCC is not fully understood. However, recent studies may indicate that alterations by HBV to the cellular metabolism could be one of the factors that lead to hepatocyte transformation. In our lab, we are trying to address this question by focusing on glucose metabolism using primary rat hepatocytes (PRHs) and recombinant adenovirus infection model system. We show that AdHBV infected PRHs have an increased glucose uptake rate as compared to the controls. We also see an effect of varying glucose concentration on HBcAg (HBV core protein) levels and on HBV replication, suggesting a major role of glucose utilization on viral pathogenesis.

Furthermore, to understand how glucose is being utilized by the hepatocytes to favor HBV, we would like to propose that upregulation of glucose uptake could be mediated by PKM2 (pyruvate kinase M2)/HIF1a (hypoxia inducible factor 1a) axis, which is one of the most commonly activated pathways in cancers, wherein glucose is then subsequently shunted towards anabolic PPP (pentose phosphate pathway) generating excess nucleic acids required for viral replication.

Understanding how HBV manipulates cellular activities that subsequently cause HCC may reveal some new potential therapeutic targets.

Andrea Rosenkranz

Bouchard Lab Member: Andrea Rosenkranz

An estimated 240 million people worldwide are chronically infected with hepatitis B virus (HBV). Chronic HBV infections often lead to the development hepatocellular carcinoma (HCC) and liver cirrhosis. Currently, there is a prophylactic vaccine that many of us receive in order to prevent infection and chronic disease; however, HBV has remained a serious health concern in some areas of the world. Moreover, there is no cure for chronic HBV infection.

Recent studies regarding the mechanism of entry for HBV infection have shed light on new therapeutic targets, such as the sodium taurocholate co-transporting polypeptide (NTCP), which is required for viral infection. My research aims to further elucidate the mechanisms by which viral entry and infection occur and more specifically the mechanism of fusion. To date, there is very little understood regarding the entry mechanism of HBV. Previous studies have shown that there is a likely fusion peptide at the N-terminus of the small surface protein, which is required for viral entry. Additionally, a portion of the large surface protein may play a role in fusion as well as a putative cholesterol recognition/interaction amino acid consensus (CRAC) domain, which may help stabilize binding of the HBV surface proteins to the host cell receptors.

Using a combination of structural studies and molecular biology approaches, I hope to gain new insight into the structural rearrangements and virion and host cell requirements that contribute to the fusion process.

Current Rotation Students

Kyle Yeakle
Rama Karadsheh
Marwaa Lalusi
Simran Shamith
Lilly Oni

Members of the Bouchard Lab

Lab Alumni

Bouchard Lab Alumni

John Allsop

Brooke Morsell

Danyelle Paine

Tara Dolchin

Raviteja Bethamcharla

Laura Martin Conde (Spain 2019)

Amaya Genovia

Katie Huynh

Michael Owens

Ryan Pearson

Sumedha Bagga


Jessica Casciano

Jason Lamontagne

Siddhartha Rawat

Emre Yetkin

Yi Guo

Gregory Piech

Amy Clippinger

Tricia Gearhart

Bei Yang

Stephanie McClain

Rebecca Lizzano

David Randolph

Anthony Bustamante

Juan Canas

Matthew Dorazio

Kyle Keinath

Mallory Zvarick

Lyali Al-seed

Hanadi Qashqari

Natalia Ross (Spain 2011)

Romain Deltour (France 2016)

Nick Duchemin

Khin Zar Win Pyae

Conor O'Meara

Anthony Phandinh

Alyssa Duffy

Rebecca Genovese

Haley Majer

Jone Urcelay (Spain 2017)

Richa Pande

Daniel Slusaw

Theodore Gurrola

Lisa Grimaud (France 2018)

Elodie Dubois (France 2018)

Paula Jimenez (Spain 2018)

Jake Parfianowiez

Justus Martin

Srinidhi Baile

Pearson Brooks

Clemence Prette (France 2017)

Eric Halijasmaa

Ahsun Bajwa

Allison Yankee

Michael Owens

Bouchard Lab Members and Alumni

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Images from the Bouchard Lab at Drexel University College of Medicine.