Hydroxychloroquine: Effective, but many side effects including prolonged QTC interval possibly dangerous in patients with hypertension and low ejection fractions.
Remdesivir: Currently undergoing trials
Tocilizumab: Currently undergoing trials
Convalescent Plasma: determined to be a promising treatment, however the supply of plasma as the ratio of cured individuals to sick patients is extremely low. Convalescent plasma therapy is a labor-intensive therapy, and in a time of pandemic, may not be the most economically viable treatment available. This type of therapy is widely known to be effective.
Note: All dates on all linked articles are in ISO YYYY-MM-DD format. All articles are to be sorted by oldest-first and formatted with the title in italics, date in bold with parentheses, and URL in brackets.[/SPOILER]
SECTION II: Pathology
Section II-A: Transmission & Strains
There is a lot of conflicting information on R0 values for COVID-19. In one epidemiological study, the disease was estimated to have a peak R0, the reproduction value, of around 6.6, which means 1 person infects that many other people, on average. One Belgian scientist said it was between 4.7 to 7. In various other locations and studies, the R0 was calculated at around 2 to 3, largely because of differences in population density and public transport use. In other words, the R0 has been variously calculated as being somewhere between 2 and 7. In some locales, the R0 may vary depending on human behavior. There are also super-spreader incidents where one person can infect dozens of others:
SARS-CoV-2 is apparently airborne and can linger in aerosols for a very long time. One study in China indicated that the virus could travel as far as 4.5 meters/15 feet, rendering the CDC’s 6-foot gap provision insufficient:
SARS-CoV is known to have spread by the oral-fecal route and through airborne sewage particulate matter, and SARS-CoV-2 is likely no different in that regard. SARS causes enteric symptoms and contaminates sewers and makes them hazardous:
SARS-CoV-2 is capable of asymptomatic transmission and it is practically impossible to stop the spread by contact tracing and minor quarantines. There are a multitude of asymptomatic carriers walking around:
SARS-CoV-2 can enter the eye through the ocular surface. Any protective mask must be full-face. Half-face masks are insufficient. Conjunctivitis can be a sign of infection:
The virus binds to ACE2 receptors in human cells. ACE2 receptors are found in many vital organs and reproductive tissues in the human body. Lungs, heart, kidneys, brain. SARS-CoV-2 infection may also have negative effects on male fertility. ACE2 receptors are found in the seminiferous ducts of the testis:
When the virus binds to ACE2 receptors, it blocks off the ACE2 receptors and leaves excess circulating Angiotensin II (normally, Ang II uses ACE2 to convert into Ang 1-7, a MasR agonist). This goes on to cause inflammation and possibly even hypertension and/or electrolyte imbalance:
SARS-CoV has been shown to be capable of Dengue-like antibody-dependent enhancement, tricking the immune system into aiding the virus. It is unknown whether or not SARS-CoV-2 can do the same:
Angiotensin blockers (ARBs), like Losartan and Telmisartan may have unwanted side effects, like increasing the number of host cell receptors that the virus can use. Generally, patients treated with ARBs have higher concentrations of ACE2 receptors on pulmonary, etc. Epithelial cells, increasing the efficacy of host cell binding. Some conflicting information indicates that they may also block the effects of the virus, leaving open the possibility of their use in therapy. Whether or not ARBs are safe to use on COVID-19 patients remains a matter of some dispute:
SARS-CoV-2 can potentially cause irreversible lung fibrosis and chronic lung disease if not caught and treated with antivirals at an early stage. This has serious implications for treatment of recovered patients who subsequently get infected with a different strain; their weakened condition may increase mortality. One COVID-19 victim had such severe damage to their lungs, they needed to be treated with a double lung transplant:
SARS-CoV-2 can potentially cause myocarditis leading to myoglobin accumulation in the blood, cardiomyopathy, and cardiac or renal failure. Some contradictory studies indicate heart tissue remains mostly normal under histopathological examination, while others indicate severe myocarditis:
SARS-CoV has been known to cause vasculitis of the organs, possibly by attacking blood vessels directly. It is unknown whether or not this also applies to SARS-CoV-2. Substantially more research is needed on this topic:
SARS-CoV (a relative of SARS-CoV-2) has been shown to cause neural death (surprisingly without encephalitis) in transgenic mouse models. Recent, concerning reports of anosmia in COVID-19 patients may perhaps indicate olfactory nerve infiltration or inflammation of the surrounding tissues; this needs investigation:
Recent information seems to suggest that SARS-CoV-2 can cause neurological symptoms and cerebrovascular disease, leading to loss of autonomic functions of the brain and, in the worst case, lingering brain damage. The virus can apparently attack the medulla or even cause viral encephalitis, and some patients have had the virus found in their cerebrospinal fluid:
COVID-19 can also possibly cause massive co-infections of prevotella, a normally harmless gut bacteria, potentially even displaying bacteriophage-like synergistic behavior with prevotella. The researchers seemed to have low confidence in this result, but it may be something worth following up on to see if SARS-CoV-2 is capable of bacteriophage-like behavior in vitro. Bacteriophage-like behavior, if present, could make the virus into a persistent environmental contaminant, and would have serious implications vis a vis disposal of bodies of COVID-19 victims and treatment of wastewater. However, the idea of a virus that infects both prokaryotic and eukaryotic cells is very strange:
SARS-CoV and SARS-CoV-2 can both cause cytokine storms, where inflammatory agents released by the body's own immune system begin to over-accumulate and damage tissues that they were sent to protect: