COVID-19 & Random unsuccessful(or partially successful)applications of Antivirals, Immunomodulators, Plasmatherapy actually open up The great limitations of Specific Protocolised(Copy & Paste) treatment procedures. It also create a hindrance to Vaccination part by forceful pathogenic mutation.
There is nobody to protest these, nobody to say ” Continious administration of Remdesivir, Flavipiravir, HCQ are actually compel the pathogen to mutate of its enzymatic components, which create a great faliure in preparing the vaccine of the same, not only that it makes also hindrance of making Host-Pathogen relationship, which is main components of developing Herd Immunity “.
Whole world are running behind such a pathogen, which is highly adaptable in nature.Respect to all ongoing curative & prophylactic approaches, all the forward movement, bullseyeing the viral molecular structure are going in vain due to its high mutatic nature. Rather we force the the pathogen to again rapid mutation,by continious trial of different antivirals & other methods.
THE ONGOING TREATMENT PROCEDURES AND THE LIMITATIONS:-
A. ANTIVIRALS/ANTI MICROBIALS
B. IMMUNOMODULATION- TO REDUCE CYTOKINE STORM
C. PLASMA THERAPY
A. ANTIVIRALS/ANTIMICROBIALS-
Currently there is no specific antiviral treatment for COVID-19. An antiviral drug must be able to target the specific part of a virus’s life cycle that is necessary for it to reproduce. In addition, an antiviral drug must be able to kill a virus without killing the human cell it occupies. And viruses are highly adaptive. Because they reproduce so rapidly, they have plenty of opportunity to mutate (change their genetic information) with each new generation, potentially developing resistance to whatever drugs we develop.
Remdesivir-
the coronavirus that causes COVID-19 is similar to the coronaviruses that caused the diseases SARS and MERS — and evidence from laboratory and animal studies suggests that Remdesivir may help limit the reproduction and spread of these viruses in the body. In particular, there is a critical part of all three viruses that can be targeted by drugs. That critical part, which makes an important enzyme that the virus needs to reproduce, is virtually identical in all three coronaviruses; drugs like Remdesivir that successfully hit that target in the viruses that cause SARS and MERS are likely to work against the COVID-19 virus. Remdesivir was developed to treat several other severe viral diseases, including the disease caused by Ebola virus (not a coronavirus). It works by inhibiting the ability of the coronavirus to reproduce and make copies of itself: if it can’t reproduce, it can’t make copies that spread and infect other cells and other parts of the body.
EIDD-2801-
The drug might even be more efficient at blocking the novel coronavirus, SARS-CoV-2, than Remdesivir, a drug being tested against COVID-19 in clinical trials that began in March. While remdesivir stops the novel coronavirus from replicating entirely, EIDD-2801 introduces genetic mutations into the virus’s RNA. As the RNA makes its copies, so many damaging mutations accumulate that the virus is no longer able to infect cells,
Favipiravir-
The antiviral drug, called favipiravir or Avigan, has been used in Japan to treat influenza, preventing from replicating
Chloroquine and Hydroxychloroquine-
It can disrupts the ability of the SARS-CoV virus to enter and replicate in human cells. SARS-CoV is closely related to the novel coronavirus, SARS-CoV-2, and caused an outbreak of severe acute respiratory syndrome in 2002. The cell culture studies of SARS-CoV-2 revealed that the drug and its derivative Hydroxychloroquine undermine the novel virus’ replication in a similar way. In combination with an antibiotic called Azithromycin , effect appeared to be amplified.
SO,WHAT IS THE CAUSE OF FAILURE TO IDENTIFY THE DRUG OF CHOICE?
-
Multiple point mutation of the virus.
-
Drugs are using on the basis of the data of its action against similar virus, not same (different in many molecular points)
-
Drugs are prepare targeting the specific part of virus’s pathogenesis (any minimal change of that causing failure of the drugs)
B. IMMUNOMODULATION- TO REDUCE CYTOKINE STORM(THE FATAL PART)
Studies suggest that for many patients who die of Covid-19, it may be their own immune system, rather than the virus itself, that deals the fatal blow. This is called a cytokine storm.
During a cytokine storm, the immune system keeps raging long after the virus is no longer a threat. It continues to release cytokines that keep the body on an exhausting full alert. In their misguided bid to keep the body safe, these cytokines attack multiple organs including the lungs and liver, leading to Acute Respiratory Distress Syndrome(ARDS) and Multi-Organ Dysfunction Syndrome(MODS).
Untreated, cytokine storm syndrome is usually fatal. In treating cytokine storms brought about by other illnesses, like other viral infections and autoimmune diseases, death rates among patients suffering a cytokine storm have been reduced to as low as 27%.
A patient battling a cytokine storm may have an abnormally fast heart rate, fever and a drop in blood pressure.
Apart from a surge in interleukin-6, the body may also show high swirling levels of molecules called interleukin-1, interferon-gamma, C-reactive protein and tumor necrosis factor-alpha.
There is a relatively simple, rapid and easily available test that can detect whether a patient’s body has been taken over by a cytokine storm. It looks for high levels of a protein called Ferritin.
MEDICINE USING TO COMBAT THIS-
Tocilizumab-
It mutes the activity of a specific cytokine called interleukin-6 that is associated with an over-exuberant immune response.
Anakinra-
It mutes interleukin-1, another of the wayward proteins.
Hydroxychloroquine-
a much-spotlighted malaria drug(discussed above) that also calms an overactive immune response.
SO,WHAT IS THE CAUSE OF FAILURE:-
Again the drugs are using to combat it are CYTOKINE SPECIFIC. There are many types of cytokine present in our system & which type is coming in role is not only depend on virus but depend on the affected individual also. So, the various mutatic changes in virus & its host response variety causing failure of the above CYTOKINE SPECIFIC DRUGS.
C.PLASMATHERAPY-
When people recover from COVID-19, their blood contains antibodies that their bodies produced to fight the coronavirus and help them get well. Antibodies (IgG & IgM anti-SARS-COV-2)are found in convalescent plasma, a component of blood. Convalescent plasma — literally plasma from recovered patients .In order to donate plasma, a person must meet several criteria. They have to have tested positive for COVID-19, recovered, have no symptoms for 14 days, currently test negative for COVID-19, and have high enough antibody levels in their plasma. A donor and patient must also have compatible blood types.
SO,WHAT IS THE LIMITATIONS:-
The main limitation is this individual convalescent plasma units demonstrate DONAR-DEPENDANT VARIABILITY in antibody specificity and titre,that would be not beneficial of another COVID positive individual in all cases.
Secondly, donar should get a natural recovery from COVID without any medicines, otherwise the antibody titre become a COMPROMISED one.The practicability of this under question mark.
Other many TRANSFUSAN HAZARDS & confusion on the TIME OF INITIAION OF TREATMENT are also there.
© 2020 Dr. Sourav Kumar Paul. All rights reserved.
