Template:COVID-19 Testing, Reporting, and Information Management in the Laboratory/Overview of COVID-19 and its challenges/Challenges of managing the disease in the human population

1.3 Challenges of managing the disease in the human population

The graphical abstract from Li et al. 2020, showing general features of SARS-CoV-2, current knowledge of molecular immune pathogenesis, and diagnosis methods of COVID-19 based on present understanding of SARS-CoV and MERS-CoV viral infections

COVID-19 has presented numerous societal challenges, from supply line interruptions and economic sagging to overwhelmed healthcare systems and civil disorder. However, these are largely the social, economic, and political ripple effects of a disease that has brought with it a set of inherent attributes that make it more difficult to manage in human populations than say the flu.

However, COVID-19 is not the flu, and it is indeed worse in its effects than the flu, contrary to many people's perceptions. Yes, COVID-19 and the flu have some symptom overlap. Yes, COVID-19 and the flu have some transmission type overlap. But from there it diverges. COVID-19 is different in that it is more prone to be transmitted to others during the presymptomatic phase. And the body of evidence has grown since April that SARS-CoV-2 is transmittable in other ways, such as an airborne route. Hospitalization rates are higher, perhaps up to 10 times higher than the flu, and hospital stays are longer with COVID-19. People are dying more often from COVID-19 too, up to 10 times more often than people stricken with the flu. And of course, whereas people have been acquiring the flu vaccine yearly, limiting the percentage of the population that becomes ill, there is yet no vaccine for COVID-19, meaning everyone is susceptible.

Other aspects of the disease that make this difficult to manage include:

• Median incubation period: According to research published in Annals of Internal Medicine, the median (i.e., the central tendency, which is less skewed than average) incubation period is 5.1 days, with 97.5% of symptomatic carriers showing symptoms within 11.5 days. The authors found this to be compatible with U.S. government recommendations of monitored 14-day self-quarantines if individuals were at risk of exposure. However, many people continue to not take self-quarantines and other forms of social distancing seriously, and presymptomatic (and asymptomatic) carriers are thus more prone to spreading the virus.

• Presymptomatic and asymptomatic virus shedding: As mentioned in the previous point, carriers can be contagious during the presymptomatic phase of the disease, even while remaining symptom-free. (Rough estimates appear to indicate that anywhere between 25 to 45 percent of infected people may go without any recognizable symptoms after infection occurs.) This contagion is a result of what's called viral shedding, when the virus moves from cell to cell following successful reproduction. When the virus is in this state, it can be actively found in a carrier's body fluids, excrement, and other sources. Depending on the virus, the virus can then be introduced to another person via those sources. In the case of COVID-19, the route of transmission is still being studied, though water droplets (from sneezes, cough, talking, etc.) and potentially even aerosolized water droplets (water droplets from the body that have become fine spray or suspension in the air) are likely sources. This initial uncertainty of transmission routes, along with mixed messages early on about masks and their effectiveness for COVID-19, makes social distancing an even stronger necessity to limit community transmission of the disease.

• Understanding of high viral loads and infectious doses: Respiratory diseases such as influenza, SARS, and MERS see a correlation between the infectious dose amount and the severity of disease symptoms, meaning the higher the infectious dose, the worse the symptoms. Similarly, viral load—a quantification of viral genomic fragments—also tends to correlate with clinical symptoms. However, we are still in the investigative stages of determining if that similarly holds true to COVID-19. Early research seem to indicate, for example, there is little difference between the viral load of those with mild or no COVID-19 symptoms and those with more severe symptoms. More research must be performed to better understand how the viral load infectious dose plays a role in transmission. Given these unknowns, social distancing, wearing masks, and other means of minimizing exposure remain the best defense against the disease.

• Cardiovascular issues: Coronaviruses and their accompanying respiratory infections are known to complicate issues of the cardiovascular system, which in turn may "increase the incidence and severity" of infectious diseases such as SARS and COVID-19. While the exact cardiac effect COVID-19 has on patients is still unknown, suspicion is those with "hypertension, diabetes, and diagnosed cardiovascular disease" may be more prone to having cardiovascular complications from the disease. Current thinking is SARS-CoV-2 either attacks heart tissues, causing myocardial dysfunction, or inevitably causes heart failure through a "cytokine storm,", an overproduction of signaling molecules that promote inflammation by white blood cells (leukocytes). What's scary is that like the 1918 Spanish flu, SARS, and other epidemics, some otherwise healthy patients' immune responses are entirely overreactive, leading to acute respiratory distress syndrome (ARDS) or heart failure. Additionally, as the disease has progressed, medical professionals have noted two additional cardiovascular issues. First, an atypical amount of blood clotting has shown up in some infected patients, which may or may not be related to overreactive immune systems and underlying health conditions. Second, what is being called pediatric multisystem inflammatory syndrome (PMIS) is beginning to show up in children after the infection has passed, characterized by inflamed blood vessels and toxic shock syndrome. While research is ongoing to determine whether these seemingly hyperactive cardiovascular responses are directly linked to the virus or if virus-independent immunopathology is responsible, these uncertainties only emphasize the level of difficulty of properly treating COVID-19.