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Written by Super User

Published: 12 April 2020

CORONA VIRUS (COVID 19), A SUMMARY

The Covid-19 virus is a single stranded RNA (ribonucleic acid) positive strand, this means that the virus does not need a host system to replicate itself.  The virus attaches to ACE II and AT1 receptors located throughout the body and once attached, replicates itself inside the host cells. The incubation period of the virus is 3 to 7 days but can range up to 24 days. The larger the virus load to the body, the greater the virulence factor.  

The age of a person is the most important factor: 20 to 35% of the population are asymptomatic and may spread the disease. The elderly population with comorbid diseases and that are immune-compromised represent 30 to 65% of cases with ICU admission. The men are slightly more affected than woman, with a median age of 66 years old, and cardiac arrhythmias being the most prominent cause of death. Prognostic factors can be associated to the comorbidity of mental stress, including isolation due to quarantine measures, which may lead to depression, anxiety, psychosis and suicidality. 

Predisposing occupational factors as health care workers, caregivers, ER, paramedics, and nurses are high risk.  Persons with chronic medical conditions such as obesity, asthma, COPD, HIV, diabetes among other immune deficiencies should be considered also a high risk. In the United States preliminary studies show Hispanics and African Americans minorities are more predisposed to Covid-19.

The main symptoms in order of frequency are shortness of breath, dry cough, sore throat, loss of taste, smell, fever, body aches, diarrhea, weakness and fatigue.  These Covid-19 symptoms predispose the body’s respiratory system to go into overdrive, requiring ventilatory support. The complications arise of Acute Respiratory Distress Syndrome (ARDS) secondary to the dysfunction of the pneumocytes type II cells decreasing surfactant levels leading to decreased compliance and poor expansion of the lungs.  The condition can progress to pneumonia, septic shock, metabolic acidosis, coagulation dysfunctions and multiple organ failures leading to death.  Covid-19 may also affect the brainstem and central nervous system. 

The laboratory parameters can range from increased CPR, C-dimers, CPK, ALT, AST, Creatinine, LDH and lymphopenia.  The cytokines are also increased IL1B, ILIRA, IL7, IL8, IL9, IL10, fibroblast growth factors (FGF), granulocyte colony stimulating factors (GCSF), IP10, MCP1, MIP1B, TNF, VEGF, IL5, IL12, p70, IL15. The patients requiring intensive care units have a positive correlation with increased IL2, IL7, IL10, GCSF, IP10, mitochondria pyruvate carrier (MPC1), MIPIA and TNF. The primitive immune response causing a “cytokine storm” is the main cause of ARDS. The release of free radicals causes the multiple organ damages and or failure.

The early diagnosis gold standard is viral RNA isolation with +RT-PCR testing however, there are high false positives results with this test.  As the disease progress, a CT Scan can demonstrate an “irregular ground glass” appearance affecting both lower lobes early on, this then progresses to a bilateral diffusion with consolidation of both lobes, at a later stage. On physical examination patients may only show positive shortness of breath, rales in lungs and dullness to percussion.

Preventive active measures are below:

1-Avoid contact with surfaces infected by Covid-19 droplets from sneezing, coughing or touching, aerosol transmission from air droplets and oral transmission from feces.

2-Wash hands for at least 30 seconds, spray surfaces without wiping off with Lysol or Bleach products or cleaning products with at least 70% alcohol.

3-All high-risk frontline healthcare workers, caregivers, family members in isolation need to protect themselves by social distancing at least 6-10 feet, wear N-95 masks, gloves, gowns, and eye shields. Note: N-95 masks penetration of the virus is low, all other masks the virus can penetrate.

4-Ultraviolet rays, heating 56 Celsius degree for approximately 30 minutes, 75% ethanol, chlorine disinfectants can inactivate the virus.

Preventive dietary measures are below;

1-Home cooking is important, diets base in proteins, vegetables and fruits increase immune systems, those diets based on carbohydrate and sugar tend not to improve the immune system.

2-Supplements such as Zinc, Vitamin C, B complexes, and Melatonin may be useful.

3-Elderly population and those with comorbid diseases such as diabetes, cardiac and immunodeficient among others should take supplements.

Possible intervention drug therapies are below:

1-Chlorquinine an old and researched malarial drug made from barks of trees, Chloroquine has been shown to be capable of inhibiting the in vitro replication of several coronaviruses. Recent publications support the hypothesis that chloroquine can improve the clinical outcome of patients infected by SARS-CoV-2. The multiple molecular mechanisms by which chloroquine can achieve such results remain to be further explored. Since SARS-CoV-2 was found a few days ago to utilize the same cell surface receptor ACE2 (expressed in lung, heart, kidney and intestine) as SARS-CoV-1 (1, 2). It may be hypothesized that chloroquine also interferes with ACE2 receptor glycosylation thus preventing SARS-CoV-2 binding to target cells. Wang and Cheng reported that SARS-CoV and MERS-CoV upregulate the expression of ACE2 in lung tissue, a process that could accelerate their replication and spread (2).  Although the binding of SARS-CoV to sialic acids has not been reported so far (it is expected that Betacoronavirus adaptation to humans involves progressive loss of hemagglutinin-esterase lectin activity), if SARS-CoV-2 like other coronaviruses targets sialic acids on some cell subtypes, this interaction will be affected by chloroquine treatment (3,4). Today, preliminary data indicate that chloroquine interferes with SARS-CoV-2 attempts to acidify the lysosomes and presumably inhibits cathepsins, which require a low pH for optimal cleavage of SARS-CoV-2 spike protein (5), a prerequisite to the formation of the autophagosome. Obviously, it can be hypothesized that SARS-CoV-2 molecular crosstalk with its target cell can be altered by chloroquine through inhibition of kinases such as MAPK. Chloroquine could also interfere with proteolytic processing of the M protein and alter virion assembly and budding.  Finally, this drug could act indirectly through reducing the production of pro-inflammatory cytokines and/or by activating anti-SARS-CoV-2 CD8⁺ T-cells. Chlorquinine is being combined with Zinc and Azithromax in research clinical trials.

2-Ivermectin is presently being researched and showing that with a single dose able to have a 5000-fold reduction in virus at 48h in cell culture.

3-Remdesivir is a 1’cyano-substitute adenoside nucleotide analog prodrug may be a better treatment but research studies are being done (5).

4-Lopinavir/Ritonavir a protease inhibitor used in HIV and hepatitis treatments may also be useful.

5-Plasma anti-body received from previously recovered patients with Covid 19.

6-No vaccine at present.

In conclusion, it’s important to understand the Covid-19 clinical presentation, implement preventive and interventional measures. The Covid-19 second wave resurgence in winter months will occur, the immunity response may or may not prevent a second infection with the virus.  The United States Center for Disease and Control (USCDC) implemented guidelines to ensure that every person maintains precautionary measures in minimizing spread. There are many factors affecting the prognosis of the Covid-19, and its long-term effects from isolation, economic fallout, unemployment, elderly populations, immunocompromised, comorbidity predisposing factors such as diabetes, high blood pressure, HIV, among others. We recommend treating Covid-19 positive symptomatic, asymptomatic or high-risk patients with any of the above interventions and maintain a continuity of care thru technology (Telemedicne) below is a suggested process flow diagram.

REFERENCES

1. Wang P.H., Cheng Y. Increasing host cellular receptor—angiotensin-converting enzyme 2 (ACE2) expression by coronavirus may facilitate 2019-nCoV infection. bioRxiv2020 Feb 27. doi:10.1101/2020.02.24.963348.

2. R. Li, S. Qiao, G. ZhangAnalysis of angiotensin-converting enzyme 2 (ACE2) from different species sheds some light on cross-species receptor usage of a novel coronavirus 2019-nCoVJ Infect (2020 Feb 21), 10.1016/j.jinf.2020.02.013

3. Q. Zeng, M.A. Langereis, A.L.W. van Vliet, E.G. Huizinga, R.J. de Groot Structure of coronavirus hemagglutinin-esterase offers insight into corona and influenza virus evolution Proc Natl Acad Sci U S A, 105 (2008), pp. 9065-9069

4. M.J.G. Bakkers, Y. Lang, L.J. Feistsma, R.J.G. Hulswit, S.A.H. de Poot, A.L.W. van Vliet, et al. Betacoronavirus adaptation to humans involved progressive loss of hemagglutinin-esterase lectin activity Cell Host Microbe, 21 (2017), pp. 356-366, 10.1016/j.chom.2017.02.008

5. G. Simmons, S. Bertram, I. Glowacka, I. Steffen, C. Chaipan, J.Agudelo, et al. Different host cell proteases activate the SARS-coronavirus spike-protein for cell–cell and virus–cell fusion Virology, 413 (2011), pp. 265-274, 10.1016/j.virol.2011.02.020

6. M. Wang, R. Cao, L. Zhang, X. Yang, J. Liu, M. Xu, et al. Remdesivir and chloroquine effectively inhibit the recently emerged novel coronavirus (2019-nCoV) in vitro

Cell Res, 30 (2020), pp. 269-271, 10.1038/s41422-020-0282-0

About the author: Dr. Julio Jane Machado is a medical doctor trained at Duke University and Wake Forest medical centers in North Carolina, worked for 7 years on hot spots with global outbreaks on ships, implemented procedures, quarantine measures and reported to U.S.C.D.C..

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Written by Bienestar Centers

Published: 24 January 2020