#117 – Stanley Perlman, M.D., Ph.D.: Insights from a coronavirus expert on COVID-19

KEYPOINTS

• 01

  A coronavirus researcher since long before COVID

  Perlman, a microbiology, immunology and paediatrics professor at the University of Iowa, has studied coronaviruses for nearly four decades. He trained as a paediatric infectious disease physician and was drawn to how viruses damage developing brains. A mouse coronavirus causes demyelination resembling multiple sclerosis, and he studied that model for about 20 years before SARS arrived. His lab now uses mouse models of SARS-CoV-1 and SARS-CoV-2. The conversation was released in late June 2020, so it reflects what was known then.

• 02

  What makes a virus a coronavirus

  Coronaviruses are grouped by how they look under the electron microscope, how they replicate and, now, their genetic relatedness. Belonging to the family doesn't mean sharing hosts. Members infect mice, pigs, cows, cats, dogs and bats, and close relatives infect insects and snakes.

• 03

  Animal reservoirs make viruses hard to eliminate

  Measles and smallpox infect only people, which is why eliminating them is possible in theory. Most coronaviruses can cross species: MERS is a camel virus, SARS-CoV-1 jumped between animals, and SARS-CoV-2 can infect animals. Attia notes a reservoir lets a virus 'hide' outside humans even when most people are immune, as West Nile does in birds.

• 04

  SARS-CoV-1 burned out for two reasons

  It emerged from a live animal market in Guangzhou. Perlman says it was almost certainly a bat virus that spread to other animals, and up to a third of animal handlers had antibodies. It was declared eliminated in July 2003 after about 8,000 cases worldwide. It had no ongoing animal reservoir, and people weren't contagious until they were sick, so identifying and isolating cases worked.

• 05

  MERS: deadly but poorly transmissible

  MERS, in a slightly different branch of the family, kills about 35% of those diagnosed, with roughly 2,500 confirmed cases. Camels probably carried it since at least 1983, though it was found in people only in 2012. Perlman attributes the limited spread to an R0 of about 0.3. Infected workers returning to poorer countries infected no one, yet in Korea a single patient infected 186 people, mostly in hospitals.

• 06

  SARS-CoV-2 combines a cold virus with a SARS-like lung disease

  Perlman describes it as a common cold coronavirus in the upper airway plus SARS or MERS in the lungs. That combination gives it both transmissibility and severe disease. If only about one in five infected people develop pneumonia, its lethality among pneumonia cases may resemble SARS. He compares it to 1918 influenza: a few percent fatality across a huge denominator.

• 07

  Bad luck, not biology, protected us before

  Attia asks whether deadly coronaviruses are somehow bound to transmit poorly. Perlman says nothing about the biology makes a virus with SARS-CoV-2's spread and MERS's lethality unlikely. Attia calls that potential combination a five-fold disaster.

• 08

  No evidence of meaningful drift so far

  Unlike influenza, the human coronaviruses don't seem to change much, with the partial exception of OC43. Perlman said there was no evidence the new virus had changed in a way that would stop a vaccine or prior infection from protecting people.

• 09

  Immunity to coronaviruses wanes

  Antibodies and protective IgA to common cold coronaviruses fade within a year or two, unlike smallpox antibodies still measurable decades later. Perlman says no one really knows why, and that this is a key unknown for reinfection, vaccines and herd immunity.