Burton M Altura1-6*, Asefa Gebrewold1,5,6, Anthony Carella1,5,6 and Bella T Altura1,3-6
1Department of Physiology and Pharmacology, the State University of New York Downstate Medical Center, Brooklyn, New York, USA
2Department of Medicine, the State University of New York Downstate Medical Center, Brooklyn, New York, USA
3The Center for Cardiovascular and Muscle Biology, the State University of New York Downstate Medical Center, Brooklyn, New York, USA
4School of Graduate Studies in Molecular and Cellular Science, the State University of New York Downstate Medical Center, Brooklyn, New York, USA
5Bio-Defense Systems, Inc, Rockville Centre, the State University of New York Downstate Medical Center, Brooklyn, New York, USA
6Orient Biomedica, Estero, Florida, the State University of New York Downstate Medical Center, Brooklyn, New York, USA
*Corresponding Author: Burton M Altura, Department of Physiology and Pharmacology, the State University of New York Downstate Medical Center, Brooklyn, New York, USA.
Received: December 16, 2019; Published: January 08, 2020
Globally, hepatitis B infection is a major public health problem, and infected patients can remain asymptomatic for decades. Approximately 90% of the world’s population currently reside in regions of very high and intermediate hepatitis B infection [1]. These patients often, without knowing it, can transmit the virus to other family members, friends, and others carrying diverse diseases. Almost one million people /year die of complications due to infections caused by hepatitis B, including hepatocarcinomas and cirrhosis [2]. In the USA, today, there are as many as two million people living with chronic hepatitis B, who are totally unaware of their infection [3]. Interestingly, approximately 95% of the people with chronic hepatitis B infection come from intermediate/high prevalence countries, primarily due to a lack of screening [2-4]. About 260 million people worldwide are living with chronic hepatitis B infections [3-6].
Major concerns in the inflammatory events produced by hepatitis B viruses (HBV) in the liver center on the loss of immunocompetence of CD4 T-lymphocytes, CD8 T-lymphocytes, natural killer (NK) cells, Kupffer cells, and “pit cells” [4-11]. These cell types are normally “geared” to produce diverse antiviral molecules (i.e., interferons, tumor necrosis-alpha, and a number of interleukins) [7-11]. HBV not only severely hampers the production of these protective antiviral molecules, but results in reduction of these critical cell types in the liver [7,10,11]. So, in our opinion, any effective therapeutic measures against HBV infections, and the sequelae of events leading to cirrhosis and/or hepatocarcinomas, should focus on restoring these vital cell types and their immunocompetence, and thus prevent initiation of inflammatory events in the liver.
Citation: Burton M Altura., et al. “Could Hdfx Ameliorate the Infections and Potential Courses of Hepatocarcinomas and Cirrhosis Induced by Hepatitis B". Acta Scientific Microbiology 3.2 (2020): 31-33.
Copyright: © 2020 Burton M Altura., 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.