Why is temperature sensitivity important for the success of common respiratory viruses?

Abstract

Summary This review explores the idea that temperature sensitivity is an important factor in determining the success of respiratory viruses as human parasites. The review discusses several questions. What is viral temperature sensitivity? At what range of temperatures are common respiratory viruses sensitive? What is the mechanism for their temperature sensitivity? What is the range of temperature along the human airway? What is it that makes respiratory viruses such successful parasites of the human airway? What is the role of temperature sensitivity in respiratory zoonoses? A definition of temperature sensitivity is proposed, as “the property of a virus to replicate poorly or not at all, at the normal body temperature of the host (restrictive temperature), but to replicate well at the lower temperatures found in the upper airway of the host (permissive temperature).” Temperature sensitivity may influence the success of a respiratory virus in several ways. Firstly; by restricting the infection to the upper airways and reducing the chance of systemic infection that may reduce host mobility and increase mortality, and thus limit the spread of the virus. Secondly; by causing a mild upper airway illness with a limited immune response compared to systemic infection, which means that persistent herd immunity does not develop to the same extent as with systemic infections, and re‐infection may occur later. Thirdly; infection of the upper airway triggers local reflex rhinorrhea, coughing and sneezing which aid the exit of the virus from the host and the spread of infection in the community.

The role of nasal congestion as a defence against respiratory viruses

“…The common respiratory viruses are temperature sensitive and replicate well at the normal temperature of the nasal mucosa (32 o C) and poorly or not at all at body temperature (37 o C) (16) . This review proposes that unilateral nasal congestion and obstruction associated with the nasal cycle is a mechanism of defence against infection with respiratory viruses as it raises the nasal mucosal temperature to a restrictive temperature of 37 o C. The nasal cycle allows nasal breathing to continue at normal levels of ventilation even though one nasal passage may be obstructed as illustrated in Fig.…”

“…All common respiratory viruses replicate best at a temperature close to that of the human upper airway which is between 32 o C-34 o C (16) . Viral temperature sensitivity has been defined as follows;…”

Temperature Dependent Viral Tropism (TDVT): Understanding Viral Seasonality and Pathogenicity as Applied to the Avoidance and Treatment of Endemic Viral Respiratory Illnesses

“…The full hypothesis was proposed by Shaw Stewart and discussed at length in 2016, focusing on seasonality and the natural selection of strains with varying degrees of thermal sensitivity and pathogenicity [31]. The same hypothesis was put forward by Eccles in 2020, this time concentrating on the advantages of thermal sensitivity to the virus [32]. This shorter review summarizes the evidence for the hypothesis, including some recent studies, and discusses its implications for avoiding and treating respiratory illness including Covid-19.…”

The role of nasal congestion as a defence against respiratory viruses

“…A two‐year‐old child has a respiratory rate at rest of 26 breaths per minute which equals 37 000 breaths each day 15 ; thus, the airway is continuously exposed to potential infection from large volumes of inspired air. As well as providing easy entrance to the body for infection, the nose also provides an easy exit for the virus to infect other hosts 16 . Symptoms of nasal viral infection are runny nose, sneezing and cough 17 .…”

“…The symptoms are triggered by the host defensive response to the viral infection with the generation of inflammatory mediators such as bradykinin and prostaglandins that stimulate sensory nerves in the upper airway to cause reflex nasal secretions and sneezing by stimulating trigeminal nerve endings in the nose, and cough by stimulating vagal nerve endings in the larynx and trachea 18 . The host response to upper airway viral infection thus provides the exit mechanism for respiratory viruses as they are transmitted in respiratory fluid on fomites that can contaminate hands, and in airway fluid expelled as aerosols by coughs and sneezes 16 …”