As we head to the Fall season, we ready ourselves for the given round of common cold and influenza. This year, we will experience the second season of COVID-19 because of the “common cold” component of SARS-CoV-2. Over the past few months for those who follow COVID-19 closely, the terminology of “Hope-Simpson” has been added to the pandemic vocabulary similar to “flatten-the-curve” and “CFR”. The Hope-Simpson model describes the seasonal infection pattern of influenza shown below.
Because coronaviruses follow a similar seasonal infection pattern to that of influenza, the Hope-Simpson model has been applied to the seasonal infection pattern of COVID-19. Generally speaking, we know influenza infection rises during cold, dry conditions as well as humid, rainy conditions. What is the science behind these environment phenomena and could these help us better prepare for COVID-19 Season 2?
Before we continue in this nose-dive, it is important to define the various humidity terminologies. Relative humidity (RH) is a measure of the water content in air, relative to the maximum capacity of air to hold water vapor which is temperature dependent. Removing the temperature parameter, absolute humidity (AH) is the mass of water per unit volume of air. Alternatively, specific humidity (SH) is the mass of water per parcel mass of air.
Global Climate Effects
One of the descriptive works on climate factors affecting influenza infection globally was done by Viboud et al..[i] In this study, the researchers examined 78 sites globally distributed at different locations and found the following:
- Two types of environmental conditions are associated with seasonal influenza peaks: “cold-dry” (predominantly in “temperate” locations) and “humid-rainy” (predominantly in the “tropical” locations).
- For locations where monthly average SH or temperature decreases below thresholds of 11-12 g/kg or 18-21°C respectively, influenza infection peaks during the “cold-dry” months (i.e., winter) at minimal levels of SH and temperature.
- For locations where SH and temperature do not decrease below these thresholds, influenza infection peaks in months when average precipitation totals are at maximum levels and greater than 150 mm per month.
US Climate Effects
Barreca and Shimshack examined the weather and influenza mortality data for each of 359 urban counties every month between 1973–2002.[ii] Their key findings are:
- AH is a critical determinant of influenza mortality.
- Humidity levels (AH) below 6 g/kg are associated with increased influenza mortality.
- Half of the average seasonal differences in influenza mortality could be explained by seasonal differences in AH alone.
Climate Effects on Pathogen Physical-Chemical Properties
In their report, Lowen and Steel summarized the below effects of temperature and humidity on influenza virus.[iii]
- Influenza virus was found to be more stable at lower temperature.
- Influenza virus was found to be more stable at lower RH.
- Lower temperature and humidity have adverse effects on host biology / immune response to infection (described in next section).
- Evaporation of water from respiratory droplets occurs more rapidly with lower RH and increases the distance and time of transmission event (via “lighter” virus), as exemplified by the table below. [iv]
Climate Effects on Host Immune Response
In a “humidity” study by Iwasaki et al.,[v] they found low humidity impairs barrier function and innate resistance against influenza infection. Specifically, they found the following in their animal model:
- Inhalation of dry air decreases mucociliary clearance, innate antiviral defense, and tissue repair.
- Induction of IFN-stimulated genes (IFN: interferon) / innate immune response was diminished in multiple cell types.
- Disease pathology was mediated by inflammasome caspases (pro-inflammatory).
In a separate “temperature” study by Iwasaki et al.,[vi] they found temperature-dependent innate defense against the common cold limits viral replication at warm temperature. Specifically, they found the following in their animal model:
- Infected airway cells exhibited a significant enhanced expression of antiviral defense response genes at 37 °C relative to 33 °C; this higher expression of type I and type III IFN genes and IFN-stimulated genes (ISGs) was observed at 37 °C.
- Temperature-dependent IFN induction was dependent on the MAVS protein, a key signaling adaptor of the RIG-I-like receptors (RLRs).
Taken together, humidity and temperature affects the body’s immune response in the nasal passage, the first point of contact between the pathogen and the human body.
SARS-CoV-2
As presented in the White House press conference in April, the half-life data for SARS-Cov-2 is shown below, highlighting cold temperature and low humidity as preferred conditions for the virus.
The effects of temperature and humidity on the spread and mortality of COVID-19 is expected to follow the similar pattern for influenza and common cold. The practical advice is to stay warm in an environment with AH of greater than 6 g/kg or RH of 40-60%. A wool scarf and humidifier will go a long way in protecting the nose and you against the common cold, influenza, and COVID-19.
[i] doi: 10.1371/journal.ppat.1003194
[ii] doi: 10.1093/aje/kws259
[iii]doi:10.1128/JVI.03544-13
[iv] doi: 10.1098/rsif.2018.0298
[v] doi: 10.1073/pnas.1902840116
[vi] doi: 10.1073/pnas.1411030112