It seems incredible in this Age of Pandemics that a dozen broad-spectrum antiviral drugs have been largely ignored in the fight against Covid-19. This class of drugs works by inhibiting a critically important human protein called nuclear-factor kappa-binding - NF-kB for short.

NF-kB exists in the cytoplasm of every cell and does two main things related to disease. When it is released from its inhibitor I-kB, it increases both inflammation and viral replication. That is why cells carefully restrain it. Cells lock it safely away in the cytoplasm to prevent it from causing these two negative effects that occur when it is released and moves from the cytoplasm into the nucleus. When its inhibiting bond with I-kB – inhibitor of kB - is dissolved and it is released, NF-kB greatly increases both inflammation and virus production. The NF-kB release-inflammation-viral replication cycle becomes a self-reinforcing positive feedback loop. Reducing this stimulant protein, keeping it locked away, attached to its inhibitor, is important in fighting viral infections and limiting the damaging inflammation it causes. That is why NF-kB inhibitor drugs (NF-kBIs) are so important. However, during the entire Covid-19 pandemic almost no one has mentioned NF-kB or NF-kBIs except for dexamethasone and other strong anti-inflammatory steroid drugs like prednisone and hydrocortisone. These steroid drugs have serious side effects and can be used only for a limited time, about two weeks. What most people, including many doctors, do not realize is that these commonly known anti-inflammatory drugs also work as antiviral drugs. They are dual purpose. NF-kBIs form a whole class of drugs we have failed to utilize in the past to fight viral infections. It is past time we did. Millions of lives have been lost due to this oversight.

In 1990 and 1991 Dr Donald Kotler of Columbia University published two abstracts that showed that 5-ASA, an aspirin (ASA) analogue, could inhibit HIV replication by about 65% as well as AZT, the first anti-AIDS drug. A dozen years later, research by me and Dr Elopy Sibanda, an immunologist in Zimbabwe, showed that aspirin alone could increase CD4 count twice as high and for twice as long – for one year – as AZT could. However, compared to many NF-kBIs, aspirin is relatively weak. Some NF-kBIs are dozens of times stronger than aspirin at reducing NF-kB. Thus, a whole class of drugs exists that doctors mostly have not been using to treat viral infections and save lives. NF-kBIs include both steroid and non-steroid anti-inflammatory drugs (NSAIDs). Who knew that common anti-inflammatory drugs also work as antiviral drugs? Now we do. So why are we not using them, especially when deadly viruses strike?

The main reason even doctors are not informed about this large class of variously powerful broad- spectrum antiviral drugs is that pharmaceutical companies want to develop specific antiviral drugs for each new virus that emerges so they can charge excessive prices for those new drugs, just like they did with AZT. They want to ignore or coverup the fact that relatively cheap existing drugs are somewhat effective against almost all viruses because almost all viruses stimulate the release of NF-kB to boost their own replication. NF-kB is the primary stimulant or fuel for viral replication. This becomes a self-sustaining cycle. The more NF-kB, the more virus production. The more virus, the more NF-kB is released. Physicians need to interrupt this escalating cycle. An effective way to do that is by administering NF-kB inhibitor drugs. When more specific antivirals are eventually developed, they can be added as a combination therapy.

Howard Armistead is Director of the Selenium Education and Research Centre, Johannesburg, [email protected].

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