The spread and pathology of Covid-19

The spread and pathology of Covid-19

  • Malgorzata Urbacz

Scientists have successfully modelled the transmission dynamics of SARS-CoV-2, predicting second waves and recurrent winter outbreaks.

Researchers from Harvard university have published extrapolated data which represent the likely course of coronavirus transmission rates. The information published in Science serves as a warning to healthcare organisations to prepare for a surge in cases, following a relief in social distancing.

COVID-19 has infiltrated nearly the entire globe, infecting over 8 million people and claiming over 440,000 lives worldwide. Although the coronavirus family was thought to be well-understood, COVID-19 is unique from previous SARS and MERS infections. With no effective pharmaceutical treatment, the only way to fight the virus is through social interventions such as contact tracing, quarantine and social distancing.

The global decision to adopt social distancing measures has proven successful to “flatten the curve” of transmission rates, with some countries, like China, gradually lifting the nationwide lockdown. Initially it was thought that COVID-19 would follow the same trajectory as SARS, eventually disappearing after an intense epidemic. Unfortunately, this is becoming increasingly unlikely, as China reports a sharp rise in infections following a briefly optimistic incubation period. What is now proposed, is that COVID-19 will circulate seasonally, just like the winter flu or previous human coronavirus (HCoV).

HCoV is considered to be the second most-likely cause of the common cold, diffusing through populations seemingly unnoticed in annual wintertime outbreaks. For this reason, the researchers predict that the most likely season to experience a surge in COVID-19 infections is winter. As is true for influenza, the cooler climate may facilitate the spread of infection.

The real determining factor of whether COVID-19 will enter into regular circulation, is the nature of the immunity it produces. If it is permanent, the virus will be wiped out for at least 5 years once herd immunity is achieved e.g. through vaccinations. If not permanent, it will likely circulate seasonally, possibly in annual, biennial or random patterns of emergence over the next five years. What the researchers knew already, is that betacoronaviruses (a smaller family of coronaviruses, to which COVID-19 belongs) can provide cross-immunity to each other. That is, if you are infected with HCoV you can, theoretically, be immune from COVID-19. Scientists propose that even if COVID-19 immunity is not permanent, mild cross-immunity from other betacoronaviruses may prevent the re-emergence of COVID-19 at least until 2024.

The researchers worked hard to simulate every possible post-pandemic outcome and found that social distancing only causes a reduction in transmissibility rates for its duration. In every scenario there was a resurgence in infection when the social distancing was lifted. The length of the social distancing had a surprising impact on the result, as the infection peak following a 20-week lockdown period was nearly the same as that with an uncontrolled epidemic with no distancing measures put in place. This suggests that longer lockdown periods result in a failure to build any population immunity, leaving a larger proportion of the population vulnerable to infection.

When simulating a scenario with a resurgence in COVID-19 infections during the winter, they found that transmissibility rates soared well above that of an uncontrolled epidemic. Researchers warn that with no herd immunity and a resurgence in infections, the number of critical cases will exceed the critical care capacity, meaning hospitals will inevitably be met with an overwhelming number of severely ill patients.

The scientists suggest that shorter, regular social distancing measures could prevent hospitals becoming overwhelmed. Shorter lockdown periods result in a lower resurgence peak which can be lowered again with another lockdown. Modelling with current critical care capacities, this looks to be the best way forward to prevent any rogue surges in infection rates and keep the maximum at a level which is manageable. Without any new therapeutics or vaccines, the researchers predict intermittent social distancing measures need to be maintained until 2022. Even following successful elimination of transmissibility, the situation should be monitored closely to assess the possibility of another COVID-19 infection, which could arise as late as 2025.

Reference:

Kissler S.M., Tedijanto C., Goldstein E., Grad Y.H. and Lipsitch M. (2020) Projecting the transmission dynamics of SARS-CoV-2 through the postpandemic period. Science 368(6493),860-868. Available from: DOI: 10.1126/science.abb5793

Alongside understanding the global spread of the virus, understanding the pathology is also vital. Scientists have successfully identified where and when coronavirus can be detected in the body.

Following a series of patients infected with SARS-CoV-2, researchers from Germany have created an infection profile to describe the spread of viral load throughout the body. SARS-CoV-2 is the virus responsible for the ongoing COVID-19 pandemic, first identified in Wuhan, China in late 2019. Since then it has infected over 8 million people worldwide.

It was clear from the start, that SARS-CoV-2 would follow the path of its closest genetically-related virus SARS-CoV-1 and cause respiratory distress in its host. Both of these viruses use a receptor known as angiotensin-converting-enzyme 2 (ACE2) to enter into cells, with the help of a cellular protease TMPRSS2. The target cells for the virus are found in the lungs, and when infected, become the site of viral replication. The cells eventually die and cause symptoms such as respiratory distress and pneumonia.

Although there are similarities between SARS-CoV-1 and CoV-2, there are differences which account for the unpredictability of COVID-19 infections. By following a group of patients, researchers were able to track the course the virus takes in a human body. What they found was that similarly to SARS-CoV-1, SARS-CoV-2 particles can be detected in sputum (phlegm) which indicates active viral replication in the lower airways and lungs. Surprisingly, SARS-CoV-2 could also be detected using nose and throat swab samples at the early stage of infection, in contrast to SARS-CoV-1 which is rarely detectable in these upper airways.

Evidence for SARS-CoV-2 replication in upper airways is additionally supported by the case of a patient with independent replication in the throat as opposed to the lungs. The preferential replication in upper airways also explains why sufferers of COVID-19 experience problems with taste and smell sensations. What the researchers think is, sufferers are most contagious when symptoms are still mild and resemble upper respiratory tract infections. Coughing induces viral shedding which can then become air-borne and infect others. Only later does the virus spread to the lower respiratory tract and resemble SARS-CoV-1 infections, eventually leading to pneumonia and lung failure.