Ephedra, an ancient herb, is applied to treat common cold and influenza for such a long time in China. Pseudoephedrine is a main active ingredient from Ephedra which is used for relieving nasal congestion clinically. We previously reported that pseudoephedrine showed a potent anti-inflammatory effect other than sympathomimetic effects. In the present study, we aimed to investigate whether pseudoephedrine could protect mice from the H1N1 virus infection. The mice were infected with a 20% LD50 influenza A virus (IAV) suspension via intranasal administration to establish a virus infection model. Further, the mice were orally administered pseudoephedrine or oseltamivir for 4 days from one day after infection. Our results showed that pseudoephedrine improved lung pathological damage during the IVA infection period, and it dramatically increased the survival rate and attenuated loss of body weight compared with the virus-infected control group. In addition, pseudoephedrine inhibited the cytokine storms and mRNAs expression of the TLR7 signaling pathway. Surprisingly, pseudoephedrine showed an inhibitory effect on the replication of IAV. These results give clear evidence that pseudoephedrine is a potential anti-influenza drug by blunting cytokine storms and inhibition of replication of IAV, and following these results, we speculate that it should be tested in the novel coronavirus pneumonia (COVID-19, a severe epidemic in China currently) in which the cytokine storms play a key role to damage bronchi and lung in the early stage.

Research on psychological risk factors for upper respiratory tract illnesses (URTIs) has been conducted for over fifty years. Early studies failed to control for exposure and also often relied on self-report rather than clinical and virological assessment. A universal policy used in the current COVID-19 pandemic has been to restrict exposure by social isolation. This leads to increased stress and removal of social interaction. In addition, information overload about the disease, and incorrect information, can also reduce wellbeing. Studies of experimentally-induced URTIs have shown that stress increases susceptibility to infection. Other research has shown that stress due to job insecurity and few social contacts are key risk factors for infection. This suggests that while social isolation will reduce exposure, it will also lead to an increased risk of illnesses, due to increased stress and reduced social support, should the person become infected with the virus. Other research has shown that infection and illness lead to changes in behaviour. These effects include greater negative affect and impaired attention and slower speed of response. Such effects are not only present when the person is symptomatic but also occur with sub-clinical infections, during the incubation period and after the illness. People with the illness are also more sensitive to other negative influences such as fatigue, and this has implications for safety critical jobs such as those carried out by healthcare professionals treating those with COVID-19.

COVID-19 virus structural components: The 2019-nCoV, also called SARS-CoV-2, was first reported in Wuhan, China in December 2019. The disease was named Coronavirus Disease 2019 (COVID-19) and the virus responsible for it as the COVID-19 virus, respectively, by WHO. The 2019-nCoV has a round, elliptic or pleomorphic form with a diameter of 60–140 nm. It has single-stranded RNA genome containing 29891 nucleotides, a lipid shell, and spike, envelope, membrane and hemagglutinin-esterase (HE) proteins. Steps in progression of COVID-19 illness: Once inside the airways, the S protein on the viral surface recognizes and mediates the attachment to host ACE-2 receptors and gains access to endoplasmic reticulum. The HE protein facilitates the S protein-mediated cell entry and virus spread through the mucosa, helping the virus to attack the ACE2-bearing cells lining the airways and infecting upper as well as lower respiratory tracts. With the dying cells sloughing down and filling the airways, the virus is carried deeper into the lungs. In addition, the virus is able to infect ACE2-bearing cells in other organs, including the blood vessels, gut and kidneys. With the viral infestation, the activated immune system leads to inflammation, pyrexia and pulmonary edema. The hyperactivated immune response, called cytokine storm in extreme cases, can damage various organs apart from lungs and increases susceptibility to infectious bacteria especially in those suffering from chronic diseases. The current therapeutics for COVID-19: At present, there is no specific antiviral treatment available for the disease. The milder cases may need no treatment. In moderate to severe cases, the clinical management includes infection prevention and control measures, and symptomatic and supportive care, including supplementary oxygen therapy. In the critically ill patients, mechanical ventilation is required for respiratory failure and hemodynamic support is imperative for managing circulatory failure and septic shock. Conclusion: Confusion, despair and hopes: There is no vaccine for preexposure prophylaxis or postexposure management. There are no specific approved drugs for the treatment for the disease. A number of drugs approved for other conditions as well as several investigational drugs are being canned and studied in several clinical trials for their likely role in COVID-19 prophylaxis or treatment. The future seems afflicted with dormant therapeutic options as well as faux Espoir or false hopes. As obvious, not all clinical trials will be successful, but having so many efforts in progress, some may succeed and provide a positive solution. Right now, though, confusion and despair prevail.

Background: The development of COVID-19 having been set apart as the third presentation of an exceptionally pathogenic coronavirus into the human populace after the extreme intense SARS-COV and MERS-COV in the twenty-first century. The infection itself doesn’t make a crucial commitment to mortality, anyway “cytokine storm” created by the unreasonable invulnerable reaction activated by the virus can result in a hyperinflammatory response of lung tissues and deadly lung injury, and in this way increment death rate. In this manner, immunomodulatory medications ought to likewise be remembered for treatment of COVID-19. Presentation of the hypothesis: the virus particles invade the respiratory mucosa firstly and infect other cells, triggering a series of immune responses and the production of cytokine storm in the body, which may be associated with the critical condition of COVID-19 patients. Once a cytokine storm is formed, the immune system may not be able to kill the virus, but it will certainly kill many normal cells in the lung, which will seriously damage the of lung function. Patients will have respiratory failure until they die of hypoxia. It is not yet clear what the death rate of Covid-19 will be, though the best estimate right now is that it is around 1 percent, 10 times more lethal than seasonal flu due to cytokines storm which trigger a violent attack by the immune system to the body, cause acute respiratory distress syndrome (ARDS) and multiple organ failure, and finally lead to death in severe cases of COVID-19 infection. Therefore, inhibiting cytokine storm can significantly reduce inflammatory injury in lung tissues. Pyridostigmine (PDG), cholinergic anti-inflammatory pathway (CAP) is a neural mechanism that modulates inflammation through the release of acetylcholine (ACh), resulting in decreased synthesis of inflammatory cytokines such as TNF-α and IL-1. This finding emphasis, the nervous and immune systems work collaboratively during infection and inflammation. Implications of the hypothesis: Administrations of Pyridostigmine (PDG) as cholinergic agonist inhibits the inflammatory response and lower the mortality of COVID-19 patients. Likewise, activation of the CAP during systemic inflammation down-regulates the production and release of inflammatory cytokines. 

The infectivity and pathogenesis: SARS-CoV-2, the causative agent of Covid-19, involves Angiotensin-converting enzyme 2 (ACE2) receptors on type II alveolar type 2 (AT2) cells in lungs. Apart from, the upper and lower respiratory tracts, the disease affects the gastrointestinal system prominently, as evidenced by the significant GI symptoms, early in the course of the disease. In addition, the virus infects ACE2-bearing cells in other organs including the heart and blood vessels, brain, and kidneys. Clinical features and morbidity: The clinical spectrum of COVID-19 varies from asymptomatic or pauci-symptomatic presentation to moderate to severe states characterized by respiratory failure necessitating mechanical ventilation and ICU support and those manifesting critical clinical condition with complications like sepsis, septic shock, and multiple organ dysfunction failure. The CT chest is an important tool for early identification of COVID-19 pneumonia as well as for prognostic purposes. The recovery and residual damage: The recovery and other outcomes vary depending on age and other aspects including sex, comorbidities, and genetic factors. The outlook for older adults, who account for a disproportionate share of critical disease, is unfavorable, and most of those who survive are unlikely to return to their previous level of functioning. The disease affects their long-term health and quality of life as well as brings in propensity for truncated post-disease survival. COVID-19 aftermath and follow up: The patients discharged from hospital following severe COVID-19, continue to suffer with lingering impact of the disease as well as that of the emergency treatments that saved their life. The post-infection reduced exercise tolerance and other subtle factors, like post viral fatigue syndrome, post-traumatic stress disorder, impaired concentration, delirium, and disturbed sleep-wake cycle often underly the functional impairment. In fact, there is need of step-down care and later a multidisciplinary support involving regular clinical assessment, respiratory review, physiotherapy, nutritional advice, and psychiatric support. Conclusion: The life after COVID-19: After recovery from the disease, the virus SARS-CoV-2, may persist for uncertain period. In addition, the chance of reinfection cannot be ruled out. The vitamin D supplementation may be helpful. In general, the quality of life (QOL) in ICU survivors improves but remains lower than general population levels, but most of the patients adapt well to their level of self-sufficiency and QOL. Also, the debility due to co-morbidities may further compromise the activity of daily living and QOL issues. The Age and severity of illness appear to be the major predictors of post-discharge physical functioning.

The coronavirus disease 2019 (COVID-19) pandemic, caused by the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), began in December 2019 in Wuhan, China. To date, the virus has infected roughly 5,000,000 people and caused approximately 345,000 deaths worldwide, and these numbers are increasing rapidly. Because of the rapid spread and the rising disease burden, several antiviral drugs and immunomodulators are in clinical trials, but no drugs or vaccines have yet been approved against this deadly pandemic. At present, computed tomography scanning and reverse transcription (RT)-PCR are used to diagnose COVID-19, and nanotechnology is being used to develop drugs against COVID-19. Nanotechnology also plays a role in diagnosing COVID-19. In this article, we discuss the role of nanotechnology in diagnosing and potentially treating COVID-19.

The coronavirus disease 19 (COVID-19) is a highly transmittable and pathogenic viral infection caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), which emerged in Wuhan, China and spread around the world (WHO, 2020). The genome of the SARS-CoV-2 has been reported over 80% identical to the previous human coronavirus (SARS-like bat CoV) [1]. As of May 2020, more than 5 million people have been affected worldwide with deaths amounting to 333000, the numbers increasing at an alarming rate day by day.

A respiratory outbreak of COVID-19 started from Wuhan, China and on 30 January 2020, WHO declared this infection to be epidemic, implementing public health emergency worldwide. On 11th March 2020, observing its prevalence in the whole world and WHO declared as a pandemic. Many countries completely collapse in the grip of this pandemic, as there are no effective treatments available, the precaution is the sole remedy to minimize this infection. The emergence and pandemic of SARS-CoV-2 (since the SARS-CoV in 2002 and MERS-CoV in 2012] manifest the third time outline of highly contagious and pathogenic infection with infect-ability to spread globally in the twentieth-first century. The SARS CoV-2 genome is highly identical to bat coronavirus which is considered to be the perfect natural host. This coronavirus even utilizes the same ACE2 receptor as SARS-CoV and mainly spread the infection to the respiratory tract, which evidently showed that transmission of this virus through interactions and exposures. The death toll of these infected patients is increasing day by day especially when they have prehistory fatal diseases like cardiovascular, diabetics, and respiratory diseases. In this review, we summarized and explained the research progressed and available data on epidemiology, COVID-19 phylogenetic relation and its impact of different fatal disease and their relation and discuss the precautionary methods to combat this pandemic. Moreover, the pieces of evidence of spreading the virus through pets and prevention of being spreading by copper metal endorsement.

The pandemic of Coronavirus Disease (COVID-19) caused by Severe Acute Respiratory Syndrome Coronavirus-2 (SARS-CoV-2) continues to rise around the globe. As per 15th July 2020, the World Health Organization (WHO) reported 13,119,239 confirmed COVID-19 cases along with 573,752 confirmed deaths globally.

The outbreaks and resurgence: The disease which reportedly began in the Chinese city Wuhan in November-December 2019, soon spread to various parts of the world, and was named and declared a pandemic disease by WHO. While the European countries were recovering from the epidemic, the disease took hold in the USA, the South American countries, Arabian countries, and South Asian countries, predominantly affecting Brazil, Peru, Iran, and India. Presently, many European countries are witnessing a resurgence and recurrent outbreaks of COVID-19. Spread and evolving new insights: Whereas there is workplace-related infection rise as people are returning to their offices, in other places the outbreaks are related to the people crowding and meeting care-freely and trying to resort back to their earlier way of life. The reopening of the educational facilities across the continents may make matters worse. Impact on health and healthcare: Most cases of COVID-19 infections go unnoticed and are followed by self-recovery. But what may appear good from the clinical perspective, appears to complicate epidemiological efforts to contain the outbreak. With the evolving information about the disease, there seem to be certain possible outcomes such as control and containment, or the persistence of the disease as global endemic accompanied with outbreaks and resurgent episodes. Gnetic factors linked to disease severity: With the COVID-19 pandemic, not all infected patients develop a severe respiratory illness. Further, there is a large variation in disease severity, which may be due to the genetic factors underlying the variable response to the virus. It is becoming clear that apart from the advanced age and pre-existing conditions, certain genetic constituent factors render some patients more vulnerable to the more severe forms of the diseases. Integration of virus into human genome: A significant part of the human genome is derived from viruses especially the RNA viruses. In fact, about 8 percent of the human genome is made up of endogenous retroviruses (ERVs), which are viral gene sequences that have become a permanent part of the human lineage after they infected our ancient ancestors. With this background, a novel concept emerging that if COVID-19 persists for several generations, its genetic material is projected to be integrated or assimilated into human genome. The involved mechanisms are conceptualized through the transposons or transposable elements of the SARS-CoV-2.