A Closer Look at COVID-19: A Q&A with Dr. Almaliky

From the day-to-day experiences to reflections on a return to "normal," an internist and WCFIA Associate reviews the course of COVID-19.

Rendering of Coronavirus

By Michelle Nicholasen

Both a medical internist and a scholar on Iraq and the Middle East, Dr. Muhamed Hassan Almaliky treats cardiology patients with coronavirus-related complications at the Penn Presbyterian Medical Center in Philadelphia. At the Weatherhead Center he runs an annual workshop for undergraduates on the politics of disease. We asked him for his professional opinion about the coronavirus outbreak and the international response to the disease. His answers appear as part of our series on scholarship in the time of the pandemic.

Read the second part of our interview with Dr. Almaliky in The International Response of COVID-19

Q: Describe your current day-to-day work during the COVID-19 pandemic.

A: My clinical duties still involve caring for cardiology patients whose admissions are now limited to emergent cases and cases that require life-saving cardiac procedures. However, a few patients with severe COVID on ventilators develop cardiomyopathy, heart failure, and arrhythmias, and need specific cardiac care. 

We have not yet reached the point of overwhelmed capacity where physicians from other specialties are pulled to care for COVID patients, though all are on standby. Generally, mild cases who present to the emergency room and test positive—and those with strong suspicion for the infection whose test results are still pending—are placed on one general medicine floor of the hospital and cared for by general medicine doctors, in coordination with infectious disease specialists. These are typically stable patients who do not need care besides close monitoring and supportive therapy. They constitute about half of all cases. 

The other half of cases have more severe disease and need high-flow oxygen or ventilator support and are cared for in one of our four intensive care units throughout the hospital and managed by pulmonary and critical care specialists. Severe cases denote patients whose gas exchange at the level of lower respiratory tract is impaired by extensive pneumonia, and the resulting inflammatory response we call ARDS: Acute Respiratory Distress Syndrome.

Q: If the new coronavirus is somewhat related to SARS, why was SARS so much less infectious and did not become a pandemic? In other words, why did this new coronavirus become a pandemic, but SARS did not?

A: The new virus is called SARS-CoV-2 (Severe Acute Respiratory Syndrome, Coronavirus 2) or “SARS-2,” as opposed to SARS of 2003. The current SARS-2 is almost identical to the old SARS. Both belong to the same sub-genus Betacoronavirus. SARS of 2003 behaved in a similar fashion to SARS-2. It was also a respiratory virus, transmitted from bats to humans in China, and started spreading around the world infecting over 8,000 and killing 916 (notice the 10 percent similarity in mortality to SARS-2).  

I do not think we have a convincing answer yet as to why SARS-CoV-2 [the novel coronavirus] is more infectious and more widespread globally. I can only state that any novel respiratory viral infection with no prior immunity has the potential to be a pandemic rather quickly, if the index case(s) is not detected quickly and controlled. However, factors related to the specific biological characteristics of the virus may offer explanation, such as the infective dose: the number of viruses needed to cause the disease in the exposed; viral virulence: the ability of any number of the viruses to cause damage to the infected tissues and organs; and the immune response of the infected individual. As more information becomes available on the biological qualities of this virus, we may be able to tell with more certainty why it behaves more aggressively than SARS.

Q: Some accounts say that if you are a COVID-19 patient and on a ventilator, you may have a 66 percent chance of dying, and that it’s unclear that ventilation is really helping. People die every year from influenza. How do influenza patients on vents compare to COVID patients in terms of duration/outcomes? 

A: Although young age and absence of comorbidities are not fully protective against succumbing to the infection of any clinical form or grade, the disease tends to afflict the elderly population much more, especially those with more than two preexisting conditions such as cardiovascular disease, high blood pressure, diabetes, asthma, and emphysema. Typically, older people who end up on ventilators for any reason do not do well, even for a non-COVID condition. Hence the need for older patients to have advanced directives so that in case they develop respiratory failure necessitating ventilator support they have the right to indicate DNI (Do Not Intubate) and DNR (Do Not Resuscitate) in their directives. This decision can be made by the patient’s family while the patient on life support is thought to have poor outcome. 

What we see is a surge of older patients with respiratory failure on the ventilators caused by extensive COVID pneumonia where the outcome is not expected to be different—exactly because of age and comorbidities factors. However, if the patient and the family opt for the ventilator-support approach, they must have the opportunity—given that mortality is not 100 percent and they still have a 50 percent chance of survival. Of course, this is to be taken on a case-by-case basis because of the wide heterogeneity of disease spectra in the elderly, coexisting disease conditions, and patients’ baseline functional capacities. 

I do not think data exists as far as whether influenza patients on the ventilator do better than COVID patients. However, mortality seems to be similar ranging from 1 to 10 percent. Influenza/pneumonia killed 55,000 Americans in 2017; 6,550 of them were attributed solely to influenza. What deters influenza from being a national or global disease emergency every year is the existence of vaccination (though not fully protective) that reduces the incidence of the infection and consequently death from it and renders most cases mild. Similarly, older populations tend to get influenza with higher frequency and die from it with higher frequency as well—either due to influenza pneumonia or bacterial pneumonia superimposed on the influenza viral infection. 

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Q: What is known about people who appear to be recovering from the coronavirus, then suddenly decline? 

A: The course may undulate in severity for the mild to moderate cases, but once at the point of needing high flow oxygen and/or artificial ventilation, the disease takes an entirely different course afterward, making recovery a lot more challenging. Intubation often means that pneumonia has affected more than 50 percent of the lung tissue, coupled with adverse inflammatory response that further “floods” the lungs and makes gas exchange difficult. At that point you are not only battling the virus but the inflammation (cytokine release syndrome) that causes multi-organ failure and death. This may imply the necessity to initiate active treatment early on especially for the vulnerable patients such as the elderly and patients with high risk: the compassionate use of antiviral agents as well other medications which have been shown in studies to positively alter the course of the disease. Recently, COVID-19 has been shown to cause hypercoagulability in patients with severe illness—even while recovering. This means the virus causes the blood to be “thick” and prone to clot formation. If the clot is formed in the lung (pulmonary embolism), it may cause a relapse of the disease and need for reintubation. This complication might be one of the causes of decline after apparent recovery. 

Q: Do researchers have any idea why the virus can be so mild for some and so deadly for others, assuming no other comorbidities? And now we understand the virus is more deadly for men than women. Could it be viral load, genetics, gender?

A: Distribution of diseases in the population, not only COVID-19, remains a puzzle. The same phenomenon has been noticed in seasonal influenza outbreaks. Although flu tends to be associated with high mortality among the elderly patients, we do see younger people with no comorbidities succumb to the severe form of it and even die of it. This is an area for further research where genetics and personalized medicine can help guide risk stratification among the nontraditional (unknown) high-risk patients. Gender distribution is another medical enigma that no one can offer a convincing answer to, much like many other diseases and infections. However, there is some evidence suggesting that higher viral RNA titers (concentrations from blood) are recovered from the more severe forms of COVID-19 disease, but the correlation is not consistent enough to draw a final conclusion.

Q: Absent a vaccine, it’s clear that in the US we may not get enough testing done to definitively tell us the immunity level in our country, or in our state. Add to that the difficulty of telling when a recovered person is no longer infectious. What would we need to know, or determine, before life can start returning to normal? How long do you think that would take, in your opinion? 

A: In a test-based patient population, two negative nasopharyngeal swabs performed twenty-four hours apart, along with evident resolution of symptoms such as fever and cough are sufficient indication of the cessation of infectivity. This means the individual can be released from the hospital and or home-based quarantine and assumed no longer contagious.

There is no conclusive research-based evidence that once a patient recovers, he/she cannot be infected again if rechallenged. However, the common medical wisdom derived from prior similar infectious disease and epidemic experiences indicates that immunity acquired after first exposure is reliable enough to release people back to public life—pending more research evidence and/or lab-based immune measurement. It was shown that “rhesus macaques infected with the virus did not develop reinfection following recovery and rechallenge.”

Life will not return to normal without a vaccine, which will take at least a year to complete developing and distributing on a global scale. Before that, we will have to wait for the last case in the US (or in Massachusetts) to recover and test negative, and for any random testing sample to be 100 percent negative for people to have the confidence again to resume full level of public activity. Fear of a second wave will loom for a while, even with the resolution of the last case, until a vaccine becomes available. Even when the vaccine becomes globally available, corona may still recur in small and limited outbreaks anywhere in the world, just like the flu. The vaccine will protect the vaccinated—or at least render their infection mild and protect against quick and widespread disease among the population under the logic of herd immunity.  

Image of patients with Spanish Flu

Q: Will there be subsequent waves of infection after the initial devastating first wave?

A: People often invoke the Spanish flu of the early twentieth century to raise concern. Though one cannot rule out the possibility of subsequent waves, similar fears also followed SARS, MERS, and Ebola, and ended up not materializing. Additionally, by the time this wave ends, we will have gained a substantial amount of knowledge about the virus and the disease it causes, and we will have put in place sufficient public health and other health resources in preparation for possible subsequent attacks. Also, we can consider every person who has succumbed to the illness and recovered as being “naturally vaccinated”—at least in the short term. This will generate some level of herd immunity. There might also be a few people who have gone through the course of the illness asymptomatically and have gained immunity. We will not know the extent of this without mass testing. 

Further, this pandemic may have caused change in social behavior that will last long, adding to the protection of a potential second attack. The news from China and the rest of the Asian countries is reassuring so far, though we must wait longer to see, and must continue to exercise caution in our social interaction for at least a few months following the last case, including cutting down on unnecessary international travel. We have also identified the segment of the population most vulnerable to the illness, and they will have to remain protected until a vaccine is found.

—Michelle Nicholasen, Editor and Content Producer, Weatherhead Center for International Affairs

Dr. Muhamed Hassan Almaliky is an Associate of the Weatherhead Center who runs the annual Center-sponsored “Politics of Disease” study group for Harvard undergraduates. He is a physician in the practice of internal medicine and cardiology at the University of Pennsylvania Health Systems, and a researcher on Iraq and the Middle East. He holds MPH and MPA degrees from Harvard University. 


  1. 3D rendering of coronavirus. Credit: Shutterstock

  2. Camp Funston, at Fort Riley, Kansas, during the 1918 Spanish flu pandemic. Credit: Wikimedia Commons