Figure 1: corona virus pandamic

1.6 Virology of Sars CoV-1

SARS-CoV-1 follows the replication strategy typical of the coronavirus subfamily. The primary human receptor of the virus is angiotensin-converting enzyme 2 (ACE2), first identified in 2003. Human SARS-CoV-1 appears to have had a complex history of recombination between ancestral coronaviruses that were hosted in several different animal groups. In order for recombination to happen at least two SARS-CoV-1 genomes must be present in the same host cell. Recombination may occur during genome replication when the RNA polymerase switches from one template to another (copy choice recombination).

1.7 Signs and symptoms of Sars CoV-1

SARS produces flu-like symptoms and may include fever, muscle pain, lethargy, cough, sore throat, and other nonspecific symptoms. The only symptom  common  to  all  patients  appears  to be a  fever  above 38  °C  (100  °F).  SARS  may  eventually  lead  to  shortness  of  breath  and pneumonia; either direct viral pneumonia or secondary bacterial pneumonia. The average incubation period for SARS is 4–6 days, although rarely it could be as short as 1 day or as long as 14 days.

1.8 Transmission of Sars CoV-1

The primary route of transmission for SARS-CoV is contact of the mucous membranes with respiratory droplets or fomites. While diarrhea is common in people with SARS, the fecal–oral route does not appear to be a common mode of transmission. The basic reproduction number of SARS-CoV, R0, ranges from 2 to 4 depending on different analyses. Control measures introduced in April 2003 reduced the R to 0.4.

1.9 Diagnosis of Sars CoV-1

SARS-CoV may be suspected in a patient who has: Any of the symptoms, including a fever of 38 °C (100 °F) or higher, and Either a history of: Contact (sexual or casual) with someone with a diagnosis of SARS within the last 10 days or Travel to any of the regions identified by the World Health Organization (WHO) as areas with recent local transmission of SARS. Clinical Criteria of Sars-Cov Diagnosis Early illness: equal to or more than 2 of the following: chills, rigors, myalgia, diarrhea, sore throat (self - reported or observed) Mild-to-Moderate illness: temperature of > 38 plus indications of lower respiratory tract infection (cough, dyspnea) Severe Illness: ≥1 of radiographic evidence, presence of ARDS, autopsy findings in late patients. For a case to be considered probable, a chest X-ray must be indicative for atypical pneumonia or acute respiratory  distress  syndrome.  The  WHO  has  added  the  category  of  ―laboratory  confirmed SARS". Meaning, patients who would otherwise be considered "probable" and have tested positive for SARS based on one of the approved tests (ELISA, immunofluorescence or PCR) but have not yet shown chest X-ray findings pointing to SARS (e.g. ground glass opacities, patchy consolidations unilateral) The appearance of SARS-CoV in chest  X-rays  is  not  always  uniform but generally appears as an abnormality with patchy infiltrates.

1.10 Prevention of Sars CoV-1

There is no vaccine for SARS, although immunologist Anthony Fauci mentioned that the CDC developed one and placed it in the US national stockpile. That vaccine, however, is a prototype and not field- ready as of March 2020.Clinical isolation and quarantine remain the most effective means to prevent the spread of SARS. Other preventive measures include: Hand-washing with soap and water, or use of alcohol-based hand sanitizer Disinfection of surfaces of fomites to remove viruses, Avoiding contact with bodily fluids, Washing the personal items of someone with SARS in hot, soapy water (eating utensils, dishes, bedding, etc.) Keeping children with symptoms home from school Simple hygiene measures Isolating oneself as much as possible to minimize the chances of transmission of the virus Many public health interventions were made to try to control the spread of the disease, which is mainly spread through respiratory droplets in the air, either inhaled or deposited on surfaces and subsequently transferred to a body’s mucous membranes. These interventions included earlier detection of the disease; isolation of people  who are infected; droplet and contact precautions; and the use of personal protective equipment (PPE), including masks and isolation gowns. 2017 meta-analysis found that for medical professionals wearing N-95 masks could reduce the chances of getting sick up to  80%  compared to no mask. A screening process was also put in place at airports to monitor air travel to and from affected countries. SARS-CoV is most infectious in severely ill patients, which usually occurs during the second week of illness. This delayed infectious period meant that quarantine was highly effective; people who were isolated before day five of their illness rarely transmitted the disease to others. Although no cases have been identified since 2004, as of 2017, the CDC was still working to make federal and local rapid-response guidelines and recommendations in the event of a reappearance of the virus.

1.11 Treatment of Sars CoV-1

As  SARS  is  a  viral  disease,  antibiotics  do  not  have  direct  effect  but  may  be   used against bacterial secondary infection. Treatment of SARS is mainly  supportive  with antipyretics, supplemental oxygen and mechanical ventilation as needed. While Ribavirin is commonly used to treat SARS, there seems to have little to no effect on SARS-CoV, and no impact on patient's outcomes. There is currently no proven  antiviral  therapy.  Tested  substances, include ribavirin, lopinavir, ritonavir, type I interferon, that have  thus   far   shown no conclusive contribution to the disease's course.

1.12 Vaccine of Sars CoV-1

As of 2020, there is no cure  or  protective  vaccine  for  SARS  that  has  been  shown  to  be both safe and effective in humans. According to research papers published in 2005 and 2006, the identification and development of novel vaccines and medicines to treat SARS was  a  priority for  governments  and public  health  agencies  around  the  world. In early 2004, an  early clinical trial on volunteers was planned. A major researcher’s 2016 request, however, demonstrated that no field-ready SARS vaccine had been completed because likely market- driven priorities had ended funding.

​​​​​​​1.13 Prognosis of Sars CoV-1

Several consequent reports from China on some recovered SARS patients showed severe long-time sequelae. The most typical diseases include, among other things, pulmonary fibrosis, osteoporosis, and femoral necrosis, which have led in some cases to the complete loss of working ability or even self-care ability of people who have recovered from SARS. As a result of quarantine procedures, some of the post- SARS patients have been documented as suffering  from post-traumatic stress disorder (PTSD) and major depressive disorder.

​​​​​​​1.14 Epidemiology of Sars CoV-1

SARS was a relatively rare disease; at the end of the epidemic in June 2003, the incidence was 8,422 cases with a case fatality rate (CFR) of 11%. The case fatality rate (CFR)  ranges  from  0% to  50%  depending  on  the  age  group  of  the  patient. Patients under 24 were least likely  to die (less than 1%); those 65 and older were most likely to die (over 55%). As with MERS and COVID-19, SARS resulted in significantly more deaths of males than females.  Probable cases of SARS by country or region, 1 November 2002 – 31 July 2003. After 11 July 2003, 325 Taiwanese cases were 'discarded'. Laboratory information was insufficient or incomplete for 135 of the discarded cases; 101 of these patients died. The viral outbreak can be genetically traced to a colony of cave-dwelling horseshoe bats in China's Yunnan. The SARS epidemic appears to have started in Guangdong, China, in November  2002  WHERE  the  first case was reported  that same month. The patient, a farmer from S hunde, F oshan, Guangdong, was treated in the First People's Hospital of Foshan. The patient died soon after, and no definite diagnosis was made on his cause of death. Despite taking some action to control it, Chinese government officials did not inform  the  World  Health  Organization  of  the  outbreak  until  February  2003. This lack of openness caused delays in efforts to control the epidemic, resulting in criticism of the People's Republic of China from the international community. China officially apologized for early slowness in dealing with the SARS epidemic. The outbreak first came to the attention of the international medical community on 27 November 2002, when Canada's Global Public Health Intelligence Network (GPHIN), an electronic warning system that is part of the World Health Organization's Global Outbreak Alert and Response Network (GOARN), picked up reports of a "flu outbreak" in China through Internet media monitoring and analysis and sent them to  the  WHO.  While  GPHIN's  capability  had  recently  been  upgraded  to  enable Arabic, Chinese, English, French, Russian, and Spanish translation, the system was limited to English or French in presenting this information. Thus, while the first reports of an unusual outbreak were in Chinese, an English report was not generated until 21 January 2003. The first super-spreader was admitted to the Sun Yat-sen. Memorial Hospital in Guangzhou on 31

January, which soon spread the disease to nearby hospitals. Subsequent to this, the WHO requested information from Chinese authorities on  5  and  11  December.  Despite  the  successes of the network in previous outbreaks of  diseases,  it  did  not  receive  intelligence until the media reports from China several months after the outbreak of SARS. Along with the second alert,  WHO  released  the  name,  definition,  as  well  as  an  activation  of  a  coordinated global outbreak response network that  brought  sensitive  attention  and containment procedures. By the time the WHO took action, over 500 deaths and an additional 2,000 cases had already occurred worldwide.

In early April 2003, after a prominent physician, J  iang  Yanyong,  pushed  to  report  the  danger to China, there appeared to be a change in official policy when SARS began to receive a much greater prominence in the official media. Some have directly attributed this to the death of an American teacher, James Earl Salisbury, in Hong Kong. It was around this same time that Jiang Yanyong made accusations regarding the undercounting of cases in Beijing military hospitals. After intense pressure, Chinese officials allowed international officials to investigate the situation there. This revealed problems plaguing the aging mainland Chinese healthcare system, including increasing decentralization, red tape, and inadequate communication. Many healthcare workers in the affected nations risked and lost their lives by treating patients, and trying to contain the infection before ways to prevent infection were known.

Table

1.15 ​​​​​​​Spread to other regions of Sars CoV-1

The epidemic reached the public spotlight in February 2003, when an American businessman traveling from China, Johnny Chen, became  afflicted  with  pneumonia-like  symptoms  while on a flight to Singapore. The plane stopped in Hanoi, Vietnam, where the victim died in H anoi French Hospital. Several of the medical staff who treated him soon developed the same disease despite basic hospital procedures. Italian doctor Carlo Urbani identified the threat and communicated it to WHO and the Vietnamese government; he later succumbed to the disease. The severity of the symptoms and the infection among hospital staff alarmed global health authorities, who were fearful of another emergent pneumonia epidemic. On 12 March 2003, the WHO issued a global alert, followed by a health alert by the United States Centers for Disease Control and Prevention (CDC). Local transmission of SARS took place in Toronto, Ottawa, San Francisco, Ulaanbaatar, M anila, Singapore, Taiwan, Hanoi and Hong Kong whereas within China it spread to Guangdong, Jilin, Hebei, Hubei, Shaanxi, Jiangsu, Shanxi, Tianjin, and Inner Mongolia.

The World Health Organization declared severe acute respiratory syndrome contained on 5 July 2003. In the following years, four SARS cases were reported in China between December 2003 and January 2004. There were also three separate laboratory accidents that resulted in infection. In one of these cases, an ill lab worker spread the virus to several other people. Study of live SARS specimens requires a biosafety level 3 (BSL-3) facility; some studies of inactivated SARS specimens can be done at biosafety level 2 facilities.

Figure

syndrome coronavirus 2 (SARS- COV-2) COVID-19:

Severe acute respiratory syndrome coronavirus 2 (SARS- COV-2) is the strain of coronavirus that causes  coronavirus disease  2019  (COVID-19),  the  respiratory  illness  responsible  for  the  COVID-19  pandemic.  Colloquially  known  as  simply  the  name,  2019   novel coronavirus  (2019-NCOV)  and has  also  been  called  human  coronavirus  2019  (HCoV-19   or hCoV-19). The World Health Organization declared the outbreak a Public Health Emergency of International Concern on 30 January 2020, and a pandemic on 11 March 2020. SARS-COV-2 is   a   Baltimore   class   IV   positive-sense   single-  stranded   RNA   virus    that    is contagious in humans. As described by the U.S.  National  Institutes of Health, it is the  successor to SARS-COV-1, the strain that caused the 2002– 2004 SARS outbreak. Taxonomically, SARS-COV-2 is a strain of severe acute respiratory syndrome-related coronavirus (SARSr-CoV). It is believed to have zoonotic origins and has close genetic  similarity  to  bat coronaviruses,    suggesting    it    emerged    from     a    bat-borne  virus.  There is no evidence yet to link an intermediate animal  reservoir,  such   as   a   pangolin,   to   its introduction to humans. The virus shows little genetic diversity, indicating that the spillover event introducing SARS-COV-2 to humans is likely to have occurred in late 2019. Epidemiological studies estimate each infection results in 1.4 to 1.9 new ones  when  no members of the community are immune and no preventive measures taken. The virus primarily spreads between people through close contact and via respiratory droplets produced from coughs or sneezes. It mainly enters human cells by binding to the receptor angiotensin converting enzyme 2 (ACE2).

Figure

​​​​​​​1.17 Terminology of (SARS- COV-2) COVID-19

During the initial outbreak in Wuhan, China, various names were used for the virus; some names used by different sources included the "coronavirus" or  "Wuhan  coronavirus‖. In  January  2020, the World Health Organization recommended "2019 novel  coronavirus"  (2019-  NCOV)as the provisional name for the virus. This was in accordance with WHO's 2015  guidance against using geographical locations, animal species, or groups of people in  disease and virus names. On 11 February  2020,  the  International  Committee  on  Taxonomy of Viruses adopted the official name "severe acute respiratory syndrome coronavirus 2" (SARS-COV-2). To avoid confusion with the disease SARS, the WHO sometimes refers to SARS-CoV-2 as "the COVID-19 virus" in public health communications and the name HCOV- 19 was included in some research articles. The general public often call  both  SARS-COV-2  and the disease it causes "coronavirus". U.S. President Donald Trump referred to the virus as the ―Chinese virus‖ in tweets, interviews, and White House press briefings.

​​​​​​​1.18 Virology Infection and transmission of (SARS- COV-2) COVID-19

Human-to-human transmission of SARS-COV-2 WAS confirmed on 20 January 2020, during the COVID-19 pandemic. Transmission was initially assumed to occur primarily via respiratory droplets from coughs and sneezes within a range of about 1.8 meters (6 ft.). Laser light  scattering experiments suggest  speaking  as  an  additional  mode  of  transmission.  Other studies have suggested that the virus may be airborne as well. Indirect contact via contaminated surfaces is another possible cause of infection. Preliminary research indicates that the virus may remain viable on plastic (polypropylene) and stainless steel (AISI 304) for up to three days, but does not survive on cardboard for more than one day or on copper for more than four hours; the virus is inactivated by soap, which destabilizes its lipid bilayer. Viral RNA has also been found in stool samples and semen from infected individuals.

The degree to which the virus is infectious during the incubation period is uncertain, but research has indicated that the pharynx reaches peak viral load approximately four days after infection or the first week of symptoms, and declines after. On 1 February 2020, the World Health Organization (WHO)  indicated  that  "transmission   from   asymptomatic   cases   is   likely   not  a  major  driver  of transmission".  However,  an  epidemiological   model   of   the beginning of the outbreak in  China suggested  that  "pre-symptomatic  shedding  may  be  typical among documented infections" and that  subclinical  infections  may have been the  source of a majority of infections. That may explain how out of 217 on board a cruise liner that docked at Montevideo, only 24 of 128  who  tested  positive  for  viral  RNA  showed  symptoms. Similarly, a study of ninety-four patients  hospitalized  in  January  and February 2020 estimated patients shed the greatest amount of virus two to three days before symptoms appear and that "a substantial proportion of transmission probably occurred before first symptoms in the index case‖. There is some evidence of human-to-animal transmission of SARS-COV-2, including examples in felids. Some institutions have advised  those  infected  with SARS-COV-2 to restrict contact  with animals.  In  July 2020, a  preliminary scientific paper reported that a major genetic risk factor of the COVID-19 virus was inherited from  archaic N review. Neanderthals ~60,000 years ago. The paper has yet to undergo peer

Figure

​​​​​​​1.19 Reservoir and zoonotic origin of (SARS- COV-2) COVID-19

The first known infections from the SARS-COV-2 strain were discovered in Wuhan, China. The original source of viral  transmission  to   humans   remains   unclear,   as   does whether the strain became    pathogenic before or after the spillover    event.    Because    many    of     the first individuals found to be infected by the virus were workers at the Huanan Seafood  Market,  it has been suggested that the strain might have originated from the market. However, other research indicates that visitors may have introduced the virus to the market, which then facilitated rapid  expansion  of  the  infections.  A  phylogenetic network   analysis   of   160 early coronavirus genomes sampled  from  December  2019  to  February  2020 revealed  that  the virus type most closely  related  to  the  bat  coronavirus  was  most  abundant  in  Guangdong, China, and designated type "A". The predominant type among samples from Wuhan, "B", is more distantly related to the bat coronavirus than the ancestral type "A".Research into the natural reservoir of the virus strain that caused the 2  002–2004  SARS outbreak has resulted in the discovery  of  many  SARS-like  bat  coronaviruses,  most originating in the Rhinolophus genus of horseshoe bats. Phylogenetic analysis indicates that samples taken from Rhinolophus sinicus show a resemblance of 80% to SARS-COV-2. Phylogenetic analysis also indicates that a virus from Rhinolophus affine, collected in Yunnan province and designated RATG13, has a 96% resemblance to SARS-COV-2. Bats were initially considered  to  be  the  most  likely  natural  reservoir  of SARS-COV-2,  which  means   that they harbour the virus  for  long periods of time with no pathogenic effects. Regarding the  animal source of infection into  humans,  the  differences  between  the  bat  coronavirus  sampled at the time and SARS-COV-2 suggested that humans were infected  via  an  intermediate  host.   Arinjay   Banerjee,   a   virologist   at  McMaster  University,  notes  that "the SARS virus shared 99.8% of its genome with a civet coronavirus, which is why civets were considered the source. ―Although studies had suggested some likely candidates, the number and identities of intermediate hosts remains uncertain. Nearly half of the strain's genome had a phylogenetic lineage distinct from known relatives. A phylogenetic study published in 2020 indicates that pangolins are a reservoir host of SARS-COV-2-LIKE coronaviruses. However, there is no direct  evidence  to  link  pangolins  as  an  intermediate  host  of SARS-COV-2 at  this moment. While there is scientific consensus that bats are the ultimate source of coronaviruses, it is hypothesized that a SARS-COV-2-LIKe coronavirus originated in pangolins, jumped back to bats, and then jumped to humans, resulting in SARS-COV-2. Based on whole genome sequence similarity, a pangolin coronavirus candidate strain was found to be less similar than RATG13, but more similar than other bat coronaviruses to SARS-COV-2. Therefore, based on maximum parsimony, a specific population of bats is more likely to  have  directly  transmitted SARS-COV-2 to humans than a pangolin, while an evolutionary ancestor to bats  was the source of general coronaviruses.

A metagenomics study published in 2019 had previously revealed that SARS-CoV, the strain of the virus that causes SARS, was the most widely distributed coronavirus among a sample of Sunda pangolins. On 7 February 2020, South China Agricultural University in Guangzhou announced that researchers discovered a pangolin sample with a particular coronavirus – a  single nucleic acid sequence of the virus was  "99%  similar"  to  that  of  a  protein-coding   RNA of SARS-COV-2.The authors state that  "the receptor-binding domain of the S protein  [that binds to the cell surface receptor during infection] of the newly discovered Pangolin-CoV  is virtually identical to that of  2019-NCOV,  with  one  amino  acid  difference."  Microbiologists  and  geneticists  in  Texas  have  independently   found   evidence   of assortment in coronaviruses suggesting involvement of pangolins in the origin of SARS-COV- 2.The majority of the viral RNA is related to a variation of bat coronaviruses. The spike protein appears to be a notable exception, however, possibly acquired through a more recent recombination event with  a  pangolin  coronavirus.  Structural  analysis  of  the  receptor  binding domain (RBD) and human angiotensin-converting  enzyme  2  (ACE2)  complex revealed key mutations on the RBD, such as F486 and N501, which form contacts with ACE2. These residues are found in the pangolin coronavirus.

Pangolins are protected under Chinese law, but their poaching and trading for use in traditional Chinese medicine remains common in the black market. Deforestation, wildlife farming and trade in unsanitary conditions increases the  risk  of  new  zoonotic  diseases,  biodiversity experts have warned. It is unlikely that SARS-COV-2 WAS genetically engineered. According to computational simulations on protein folding, the RBD of the spike protein of SARS-COV-2 should have unremarkable binding affinity. In actuality, however, it has very efficient binding to the human ACE2 receptor. To expose the RBD for fusion, furan proteases must first cleave the S protein. Furin proteases are abundant in the respiratory tract and lung epithelial cells. Additionally, the backbone of the virus does not resemble any previously described in scientific literature used for genetic modification. The possibility that the virus could have gained the necessary an adaptations through cell culture in a laboratory setting is challenged by scientists who assert that "the generation of the predicted O-linked glycan’s... suggest the involvement of an immune system."

​​​​​​​1.20 Phylogenetic and taxonomy of (SARS- COV-2) COVID-19

SARS-COV-2 belongs to the broad family of viruses known as coronaviruses. It is a positive- sense single-stranded RNA (+ssRNA) virus, with a single linear RNA segment. Other coronaviruses are capable of causing illnesses ranging from the common cold to more severe diseases such as Middle East respiratory syndrome (MERS, fatality rate ~34%). It  is  the  seventh known coronavirus to infect people, after 229E, NL63, OC43, HKU1, MERS-CoV, and the original SARS-CoV. Like the SARS-related coronavirus strain implicated in the 2003 SARS outbreak, SARS-COV-2 is a member of the subgenus Sarbecovirus (beta-CoV lineage B).Its RNA sequence is approximately 30,000  bases  in  length.SARS-COV-2  is unique among  known beta coronaviruses in its incorporation of a polybasic cleavage site, a characteristic known to increase Pathogenicity and transmissibility in other viruses. With a sufficient number of sequenced genomes, it is possible to reconstruct a phylogenetic tree of the mutation

history of a family of viruses. By 12  January  2020,  five  genomes  of  SARS- COV-2  had  been isolated from Wuhan and reported by the Chinese Center for Disease Control and Prevention (CCDC) and other institutions; the number of genomes increased to 42 by 30 January 2020. A phylogenetic analysis of those samples showed they were "highly related with at most seven mutations relative to a common ancestor", implying that the first human infection occurred in November or December  2019.As  of  7  May  2020,  4,690  SARS-  COV-2 genomes  sampled  on  six  continents  were publicly available. On 11 February 2020,  the International Committee on Taxonomy of Viruses announced that  according to  existing rules  that  compute  hierarchical   relationships   among   coronaviruses   on   the   basis   of   five conserved sequences of nucleic acids, the differences between what was then called 2019- NCoV and the virus strain from the 2003 SARS outbreak were insufficient to make them separate  viral  species. Therefore,  they  identified  2019-NCOV  as   a   strain   of   severe   acute respiratory syndrome-related coronavirus. In July 2020, scientists report that a more infectious SARS-COV-2 variant with spike protein variant G614 has replaced D614 as the dominant form in the pandemic.

1.21 ​​​​​​​​​​​​​​Structural biology of (SARS- COV-2) COVID-19

Each SARS-COV-2 virion is 50–200 nanometers in diameter. Like other coronaviruses, SARS-CoV-2 has four structural proteins, known as the S (spike), E (envelope),  M  (membrane),  and   N (nucleocapsid) proteins; the N protein holds the RNA genome, and the S, E, and M proteins together create the viral envelope. The spike protein,  which  has  been  imaged at the atomic level using cryogenic electron microscopy, is the protein responsible for allowing the virus to attach to and fuse with the membrane of a host cell; specifically, its S1 subunit catalyzes attachment, the S2 subunit  fusion.  Protein  modeling experiments  on the spike protein of the virus soon suggested that SARS-COV-2 has sufficient affinity to  the receptor angiotensin converting enzyme 2 (ACE2) on human cells to use them as a mechanism  of  cell  entry. By  22  January  2020,  a  group  in  China working with the full virus genome  and a group in the United States using reverse genetics methods independently and experimentally demonstrated that ACE2 could act as the receptor for SARS-COV-2.Studies have shown that SARS-COV-2 has a higher affinity to human ACE2 than the original SARS virus strain. SARS-COV-2 may also use basigin to  assist  in  cell  entry.  Initial  spike  protein  priming by transmembrane protease, serine 2 (TMPRSS2) is essential for entry  of SARS-COV-2. After a SARS-COV-2 virion attaches to a target cell, the cell's protease TMPRSS2 cuts open the spike protein of the virus, exposing a fusion peptide in the S2 subunit, and the host  receptor  ACE2.After  fusion,  an  endosome  forms  around  the virion, separating it from the rest of the host cell. The virion escapes when the pH of the endosome drops or when cathepsin, a host cysteine protease, cleaves it. The virion then releases RNA into the cell and forces the cell to produce and disseminate copies of the virus, which infect more cells.SARS- COV-2  produces  at  least  three  virulence  factors  that   promote  shedding of new virions  from host cells and inhibit immune response. Whether they include downregulation  of  ACE2, as seen in similar coronaviruses, remains under investigation (as of May 2020).Digitally colorized scanning electron micrographs of SARS-CoV-2 virions (yellow) emerging from human cells cultured in a laboratory

​​​​​​​1.24 WHO Role in (SARS- COV-2) COVID-19:

On March 11, 2020, the World Health Organization (WHO) had declared COVID-19 a pandemic because of alarming levels of its spread, severity and inaction. COVID-19 is caused by Severe Acute Respiratory Syndrome Coronavirus 2 (SARS-CoV-2), which is sufficiently genetically divergent from the closely related Severe Acute Respiratory Syndrome Coronavirus (SARS- CoV), to be considered a new human-infecting beta coronavirus. It mainly affects the respiratory tract and the illness ranges in severity from asymptomatic or mild to severe or critical disease. Although the current estimate of the case fatality rate of COVID-19 is < 5%, up to 15–18% of patients may become severe or critically ill, some of them requiring ICU care and mechanical ventilation On 26 February 2020, the WHO reported that, as new cases reportedly dropped in China but suddenly increased in Italy, Iran, and South Korea, the number of new cases outside China had exceeded the number of new cases in China for the first time. There may be substantial underreporting of cases, particularly among those with milder symptoms. Reported numbers may also reflect local decisions on whom and when to test. As an example, on 13 March 2020, the UK reported 798 confirmed cases, but health officials estimated the actual number of people infected was probably between 5,000 and 10,000. Since December 2019, a new strain of coronavirus named 2019 novel coronavirus (2019-nCoV) has been discovered in Wuhan. The prevalence of diabetes mellitus, which is a great public health issue leading to immunity inhibition and an increased incidence of infections, has been increasing over the past ten years. The aim of this research was to systematically assess the prevalence of diabetes mellitus among 2019-nCoV Since COVID-19 is a new disease, knowledge about this disease is still incomplete and evolving. Many case-control studies have shown that patients of COVID-19, who have underlying diabetes mellitus, develop a severe clinical course, and also have increased mortality. However, most of these studies have small sample size, and the data in them are heterogeneous and conflicting. In addition, the data on prevalence of diabetes in patients with COVID-19 is also not clear. Hence, this meta-analysis was conducted with the primary objective of exploring the relationship between underlying diabetes and severity and mortality of COVID-19 disease; and with the secondary objective of determining the prevalence of diabetes in patients with COVID-19.

Figure WHO Mortality rate of (SARS- COV-2)

​​​​​​​1.26 Prevention and Treatment of (SARS- COV-2) COVID-19:

Strategies for preventing transmission of the disease include overall good personal hygiene, hand washing, avoiding touching the eyes, nose or mouth with unwashed hands, coughing/sneezing into a tissue and putting the tissue directly into a dustbin. Those who may already have the infection have been advised to wear a surgical mask in public. Social distancing measures are also recommended to prevent transmission. Many governments have restricted or advised against all nonessential travel to and from countries and areas affected by the outbreak. However, the virus has reached the stage of community spread in large parts of the world. This means that the virus is spreading within communities whose members have not travelled to areas with widespread transmission. Health care providers taking care of someone who may be infected are recommended to use standard precautions, contact precautions and airborne precautions with eye protection. Contact tracing is an important method for health authorities to determine the source of an infection and to prevent further transmission. Misconceptions are circulating about how to prevent infection, for example: rinsing the nose and gargling with mouthwash are not effective. As of 13 March 2020, there is no COVID-19 vaccine though a number of organizations are working to develop one. China has banned the trading and consumption of wild animals. Ways of prevention and safety precautions are Hand wash, social distancing, respiratory hygiene’s, self-isolation, management. Evacuations of foreign citizens, travel restrictions, international aids grants funds, WHO measures for safety, Efforts to prevent spread have included travel restrictions, quarantines, curfews, event postponements and cancellations, and facility closures.

​​​​​​​1.27 Impacts of coronavirus of (SARS- COV-2) COVID-19

Social, economic, political, environmental, socio-economical, cultural and religious, education, societal. The outbreak of coronavirus disease (COVID-19) has severely affected the global and world economy. Major victims of the COVID-19 outbreak are micro, small, and medium-sized enterprises (MSMEs). This article aims to assess the impact of COVID-19 outbreak on these businesses and provide policy recommendations to help MSMEs in reducing business losses and survive through the crisis.

Conclusion

Suggestions are made on the possible pathophysiological mechanisms of the relationship between diabetes and COVID-19, and its management. No definite conclusions can be made based on current limited evidence. Further research regarding this relationship and its clinical management is warranted. Patients with diabetes are considered to be at higher risk for severe illness. They are more likely to need intensive care if they develop COVID-19 compared with patients who do not have diabetes and have a higher case fatality rate10, 19. Diabetes may not increase the risk of COVID-19 infection but it can lead to enhanced disease severity. Preliminary findings from the United States14 suggest that persons with underlying health conditions or other recognized risk factors for severe outcomes from respiratory infections appear to be at a higher​​​​​​​ risk for severe disease from COVID19 than are persons without these conditions. The most commonly reported conditions were diabetes mellitus, chronic lung disease and cardiovascular disease. The Centre for Evidence-Based Medicine5 states that there is little evidence on how people with diabetes can reduce their risk of COVID-19 infection beyond following general infection control guidance. Significant disruptions to routine care may also contribute to poorer outcomes during and following the pandemic. Hyperglycemia should not be overlooked, but adequately treated to improve the outcomes of COVID-19 patients with our without diabetes25. Both the HPSC1 and WHO3 highlight evidence suggesting there are two groups of people at a higher risk of acquiring a more severe disease; older people and those with an underlying medical condition such as diabetes. Clinical guidance from the CDC4 also highlights risk factors for severe illness and reports that fatality is higher for patients with diabetes. Diabetes as a distinctive comorbidity is associated with more severe disease, acute respiratory distress syndrome and increased mortality12. In a nationwide analysis on comorbidity and its impact on patients in China23, Guan et al found that the most prevalent comorbidity was hypertension followed by diabetes. The study concludes that patients with any comorbidity yielded poorer clinical outcomes than those without, and that a greater number of comorbidities also correlated with poorer clinical outcomes. Discussing two earlier CoV infections SARS and MERS Bloom garden et al34 report that regardless of the potential for the spread of COVID-19, as with influenza-reported mortality diabetes is an important risk factor for adverse outcome. Diabetes should be considered a risk factor and more intensive attention should be paid to patients with diabetes, in case of rapid deterioration.