Clinical Case Reports, Research & Trials ISSN : 2581-6756
Could A Recently-Discovered Biologic Stress Protein, HDFx, Be Useful in the Treatment and Prevention of NIPAH Infection, A New and Deadly Viral Disease?
  • Burton M. Altura* ,

    B.M. Altura, SUNY Downstate Medical Center, Brooklyn, NY; Tel No. 718-270-2194; email: burton.altura@downstate.edu

  • Bella T. Altura ,

    The Center for Cardiovascular and Muscle Research

Received: 03-08-2019

Accepted: 09-08-2019

Published: 12-08-2019

Citation: Burton M. Altura, Bella T. Altura (2019) Could A Recently-Discovered Biologic Stress Protein, HDFx, Be Useful in the Treatment and Prevention of NIPAH Infection, A New and Deadly Viral Disease?, Clin Cas Repo Rese & Trials 4: 15-19

Copyrights: © 2019, Burton M. Altura et al


Over the past decade, there has been a growing concern regarding new, emerging diseases and potential global plagues [1-4]. Since the Ebola crisis in Africa, there has been serious worries about emerging viral diseases which have no known cure or vaccine to prevent the transmission and worldwide spread of such diseases [5-7]. Ebola is one of eight viruses, termed by the World Health Organization, that is responsible for endemic and possible pandemic, concern. Recently, a new virus discovered in a Malaysian town, i.e., Nipah, was found in 1998 to be responsible for 105 deaths [6]. More recently, Nipah virus was found, in a Southern Indian town in Keralia, to have killed almost 20 people [8]. Fruit bats are prime carriers of the Nipah virus which appear to infect pigs who then transmit it to humans [9]. In 2004, the virus was found in western Bangladesh to infect people who drank palm sap contaminated by fruit bats carrying the virus [10]. There have been multiple outbreaks of the viral disease in Bangladesh and Keralia state in India where the virus appears to have been responsible for pneumonia and profound coughing and severe headaches for 7-14 days.


Although most hemorrhagic fever viruses, like Ebola, spread through bodily fluids (some cases are caused by an airborne form of the virus), it is not known if similar modes of transmission can be attributed to the Nipah virus. However, since most hemorrhagic fever viruses are known to mutate, this could happen for Nipah, hence why there is a growing concern with respect to the Nipah virus which could become infectious globally. The virus can kill at least 75% of its victims [7,10,11]. There is no known cure or preventative. Since we have recently presented evidence and posited reasons why a newly-discovered host-defense factor, i.e., HDFx, may be therapeutically, and prophylactically-effective against hemorrhagic fever viruses 12], we posit below why HDFx may also be therapeutically-effective against Nipah viral disease.


Discovery and Development of a New Biologic Host-Defense Factor, HDFx


For more than 30 years, our laboratories have been working on a new approach to develop host-defense factors that stimulate various arms of the innate and adaptive immune systems [13-19]. To this end, we have discovered a brand- new host-defense factor we have termed “HDFx”, that is a conserved protein found, so far, in rats, mice, rabbits, guinea-pigs, dogs, and sub-human primates [13, 20-29].


Approximately 135 years ago, Elie Metchnikoff, the father of immunology, hypothesized that the body under stressful circumstances, would produce powerful immunostimulants which could act on different arms of the immune system and serve to protect the host against major, dangerous insults, inflammatory conditions, and various diseases [30]. Metchnikoff’s early studies pointed to the important contributions of macrophages and phagocytic leukocytes to natural, innate resistance against pathogenic microorganisms. Over the past 40 years, considerable evidence has been brought forth to support a strong relationship between the physiological (functional ) state of the microcirculation , macrophages-phagocytic leukocytes, alveolar macrophages, , natural killer (NK) cells, the reticuloendothelial system, and “pit cells” in the liver to host defense and resistance to pathogens, hemorrhage, trauma, burns, sepsis, wounding, circulatory shock , and combined injuries [13-19,31-33].


Using Metchnikoff’s hypothesis, we posited that all of these deadly, bodily insults should produce protective factors in all surviving hosts. Indeed, we have found at least one such powerful immune stimulant we termed “HDFx” [20]. This new stress protein, HDFx, protects (to different degrees) , so far, against experimental lethal hemorrhage, lethal body trauma, lethal bacterial infections (i.e., Salmonella enteriditis, E. coli, C. welchii, among others), lethal fungal infections, combined injuries, burns, centripetal forces, and sepsis [20, 26-29,31-34].


A unique attribute of HDFx is its ability to accelerate wound healing [22].  Most importantly, it has been shown, in several animal models, to inhibit release of cytokines and chemokines, including tumor necrosis factor (TNF)-alpha, IL-6, IL-8, IL-1beta, TFN-gamma, and numerous macrophage factors [20-23, 26-29]. Thus, HDFx has the ability to ameliorate the dangerous effects of “cytokine storms” induced by both gram-negative and gram-positive microorganisms, toxic fungal organisms, hemorrhage, trauma, systemic inflammatory conditions, tissue damage, blood loss, and sepsis, among other dangerous bodily insults [20-23,26-29].


HDFx and Its Potential to Ameliorate the Deadly Effects of “Superbugs” and Possibly Nipah


Gram-negative “superbugs” appear to be major culprits in hospital-borne infections [34]. These “superbug”-induced infections seem to be more difficult to kill than gram-positive microorganisms because they are protected by “double cell membranes.  So, in order to kill the gram-negative bacteria (eg., induced by tuberculosis bacteria, diphtheria, bubonic plague, syphilis, E. coli, S. enteriditis, whooping cough, etc.) most of the approaches have been used to design antibiotics to penetrate these membrane barriers. In our opinion, another likely approach would be to engulf and digest the bacteria, fungi, and viruses and allow “supercharged” macrophages, phagocytic leukocytes, NK cells, “pit cells”, and platelets to digest and destroy these pathogenic microorganisms. But, in order for this to occur in an expeditious manner, it is our belief that the microcirculation to key organ-tissue systems (i.e., lungs, kidneys, spleen, bone marrow, heart), a drug must perforce produce optimal local tissue blood flow and distribution. Thus, an ideal drug-therapeutic agent would be to stimulate several arms of the innate immune system. To our knowledge, HDFx appears to be the only molecule that embodies all these attributes and demonstrate therapeutic qualities against numerous gram-positive, gram-negative, and diverse toxic fungal “superbug” microorganisms. Most importantly, as stated above, HDFx can accelerate wound healing in internal organs [22] that could be irreversibly damaged by toxic microorganisms like hemorrhagic fevers and emerging diseases (e.g., Ebola, Nipah, etc.).

Conclusions and Future Thoughts

It is rather obvious that the recently –discovered viral, pathogenic organism, Nipah, could wreak havoc, worldwide should this “superbug” become airborne like has happened with Ebola through mutation. This situation, in our opinion, may represent “a clear and present danger” which demands immediate action by The UN and CDC. Since the mechanism(s) of Nipah’s infectious and deadly effects are not known, and no therapy or vaccine is available to protect humans against this new “superbug’s” deadly effects, we believe HDFx should be tried against Nipah-induced infections.


Over the years, the two of us have been supported, in part, for much of our original research and ideas by several arms of The National Institutes of Health (i.e., The Heart, Lung and Blood Institute; The Mental Health Institute; The National Institute on Drug Abuse; and The National Institute on Alcoholism and Alcohol Abuse) and several major pharmaceutical companies (i.e., Sandoz Pharmaceuticals; The UpJohn Co.; Bayer Pharmaceuticals; CIBA-GEIGY Corp.; The Merck Co.; and The Warner-Lambert Co.).


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