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Role of Human Apolipoprotein E in Hepatitis B Virus Infection andMorphogenesis

Award Number: R01AI151007
ORGANIZATION: NATIONAL INSTITUTE OF ALLERGY & INFECTIOUS DISEASES
OPDIV: NIH
AWARD CLASS: DISCRETIONARY
AWARD ACTIVITY TYPE: SCIENTIFIC/HEALTH RESEARCH (INCLUDES SURVEYS)
PERIOD OF PERFORMANCE START DATE: 09/22/2020
PERIOD OF PERFORMANCE END DATE: 08/31/2026

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Role of Human Apolipoprotein E in Hepatitis B Virus Infection andMorphogenesis - Summary Hepatitis B virus (HBV) is a common cause of human liver diseases, including chronic hepatitis, steatosis, fibrosis, cirrhosis, and hepatocellular carcinoma (HCC). HBV chronically infects more than 250 million people worldwide, including 1.25 million in the United States. Although HBV vaccine has greatly contributed to the reduction of new cases of HBV infection and HCC, it does not offer therapeutic benefits to the hundreds of millions of chronic HBV carriers. The World Health Organization has called for the elimination of viral hepatitis as a public health threat by the year 2030. The biggest challenge to curing chronic hepatitis B is the elimination of HBV covalently closed circular DNA (cccDNA), which is the molecular basis for persistent HBV replication. Existing antiviral therapies with interferon and/or nucleoside analogs can effectively suppress HBV replication but do not significantly affect the level of HBV cccDNA. Thus, there is an urgent need to discover and develop new classes of antiviral drugs capable of eliminating chronic HBV infection. In this regard, a more thorough understanding of HBV infection, replication, and morphogenesis holds a great promise to identify novel targets for antiviral drug discovery and development. Through preliminary studies, we have discovered that human apolipoprotein E (apoE) is associated with infectious HBV. More importantly, our preliminary data suggest that apoE plays critical roles in both HBV infection and morphogenesis. ApoE-specific antibodies could efficiently neutralize HBV infectivity. Also, knockdown of apoE expression or knockout of apoE gene resulted in a remarkable reduction of HBV infection and production. Based on these novel findings, we hypothesize that apoE is incorporated into HBV virions and plays important roles in HBV infection and morphogenesis in vivo. The overall goal of this application is to determine the role and underlying molecular mechanisms of apoE in the promotion of HBV infection and morphogenesis in cell culture and in vivo. Our specific aims are: 1) to determine the importance of apoE in the infection and morphogenesis of clinical HBV isolates; 2) to determine apoE-binding receptors and apoE-receptor interactions important for efficient HBV infection; and 3) to illustrate the underlying molecular mechanism of apoE-mediated promotion of HBV morphogenesis. The successful completion of this application will result in a paradigm change regarding the roles of cellular proteins in HBV infection and morphogenesis. The outcomes of our studies will also provide novel molecular targets for discovery and development of antiviral drugs towards the ultimate elimination of HBV infection.


Issue Date FY	Funding FY	Legal Entity Name	Legal Entity Address	Legal Entity City	Legal Entity State	Legal Entity Zip Code	Legal Entity COUNTY	Legal Entity COUNTRY	Assistance Listing	Award Code	Budget Year	Action Date	Action Type	Action Amount

Issue Date FY: 2025 ( Subtotal = $0 )
2025	2024	WAKE FOREST UNIVERSITY HEALTH SCIENCES	MEDICAL CENTER BLVD	WINSTON SALEM	NC	27157	FORSYTH	USA	Allergy and Infectious Diseases Research	001	5	8/8/2025	CHANGE OF GRANTEE / TRAINING INSTITUTION / AWARDING INSTITUTION	$0
2025	2023	UNIVERSITY OF ALABAMA AT BIRMINGHAM	701 S 20TH STREET	BIRMINGHAM	AL	35294	JEFFERSON	USA	Allergy and Infectious Diseases Research	000	4	10/21/2024	NON-COMPETING CONTINUATION	$0
														Subtotal = $0

Issue Date FY: 2024 ( Subtotal = $438,751 )
2024	2024	WAKE FOREST UNIVERSITY HEALTH SCIENCES	MEDICAL CENTER BLVD	WINSTON SALEM	NC	27157	FORSYTH	USA	Allergy and Infectious Diseases Research	001	5	8/21/2024	CHANGE OF GRANTEE / TRAINING INSTITUTION / AWARDING INSTITUTION	$438,751
2024	2023	UNIVERSITY OF ALABAMA AT BIRMINGHAM	701 S 20TH STREET	BIRMINGHAM	AL	35294	JEFFERSON	USA	Allergy and Infectious Diseases Research	000	4	8/21/2024	NON-COMPETING CONTINUATION	$0
														Subtotal = $438,751

Issue Date FY: 2023 ( Subtotal = $420,352 )
2023	2023	UNIVERSITY OF ALABAMA AT BIRMINGHAM	701 S 20TH ST	BIRMINGHAM	AL	35294	JEFFERSON	USA	Allergy and Infectious Diseases Research	000	4	8/17/2023	NON-COMPETING CONTINUATION	$420,352
														Subtotal = $420,352

Issue Date FY: 2022 ( Subtotal = $420,352 )
2022	2022	UNIVERSITY OF ALABAMA AT BIRMINGHAM	701 S 20TH ST	BIRMINGHAM	AL	35294	JEFFERSON	USA	Allergy and Infectious Diseases Research	000	3	8/11/2022	NON-COMPETING CONTINUATION	$420,352
														Subtotal = $420,352

Issue Date FY: 2021 ( Subtotal = $420,352 )
2021	2021	UNIVERSITY OF ALABAMA AT BIRMINGHAM	701 S 20TH ST	BIRMINGHAM	AL	35294	JEFFERSON	USA	Allergy and Infectious Diseases Research	000	2	8/5/2021	NON-COMPETING CONTINUATION	$420,352
														Subtotal = $420,352

Issue Date FY: 2020 ( Subtotal = $420,352 )
2020	2020	UNIVERSITY OF ALABAMA AT BIRMINGHAM	701 S 20TH ST	BIRMINGHAM	AL	35294	JEFFERSON	USA	Allergy and Infectious Diseases Research	000	1	9/22/2020	NEW	$420,352
														Subtotal = $420,352

Grand Total All Awards = $2,120,159

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Role of Human Apolipoprotein E in Hepatitis B Virus Infection andMorphogenesis

Award Number: R01AI151007

ORGANIZATION: NATIONAL INSTITUTE OF ALLERGY & INFECTIOUS DISEASES

OPDIV: NIH

AWARD CLASS: DISCRETIONARY

AWARD ACTIVITY TYPE: SCIENTIFIC/HEALTH RESEARCH (INCLUDES SURVEYS)

PERIOD OF PERFORMANCE START DATE: 09/22/2020

PERIOD OF PERFORMANCE END DATE: 08/31/2026

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