Of late, we have heard quite a bit about systemic viruses of the nose, throat and lungs, commonly referred to as respiratory viruses. 

In this context, we’re referring to the spread of respiratory viruses beyond their expected site of infection and disease…the respiratory tract…to the blood or extra-respiratory tissues and organs, including the kidneys, liver, brain, etc. 

We tend to see this spread in the severely ill who have been infected by viruses that our body’s defences see as particularly “foreign” – not simply a “not us” kinda foreign, but more like a “hey, you usually infect small furry or feathery things, not humans!” kinda foreign.

In a recent article by Esposito and colleagues, we are reminded that this is not limited to influenza and novel coronaviruses but can be a feature of the most numerous of respiratory viruses, the human rhinoviruses (HRVs). An assumption we live by here, based on early work that made these correlations, is that viral RNA detection may approximate the detection of infectious virus at the sampling site. Some key points:

• 12% of children with HRV detected in their nasopharyngeal swabs also had virus RNA detected in their blood plasma (rhinoviraemia)
• Those children with the greatest amount of HRV RNA in their swabs also more often had rhinoviraemia
• Children with rhinoviraemia were more likely to have more severe disease. This included low oxygen saturation, high respiratory rate, white blood cell counts and C-reactive protein levels
• Children with higher viral load did not have a specific type of respiratory disease
• Viral load in the swab or plasma samples was determined by comparing to a dilution series (titration) of in vitro (lab-made) RNA.

A bit of digging in the literature will reveal that this is not a new phenomenon. There are other reports of the “common cold virus” (HRVs; I hate that term by the way) in the blood. E. Kathryn Miller and I covered some in a recent HRV-C review (From sneeze to wheeze: What we know about rhinovirus Cs). Rhinoviraemia was reported by Urquhart et al. in 1970 and 1972, by Xatzipsalti et al in children with asthma, bronchiolitis or common colds in 2005. Back in 1964, Cate et al isolated an infectious HRV from faeces. More recently, molecular tools (specifically, the polymerase chain reaction [PCR)] have been used by Tapparel et al. (2009), Harvala et al. (2012), and Lau et al. (2012) to detect HRV genome sequences in the faeces of children with fever of unknown origin, gastroenteritis, and pericarditis. In the latter case, Tapparel et al. also found HRV RNA (but not infectious virus) in pericardial and bronchoalveolar lavage fluids and plasma.

We know that even very widespread viruses, traditionally associated with mild disease, have the capacity to reach high viral loads not only at their historic site of infection, the respiratory tract, but also at disseminated sites outside the site of infection. So we’re porous!

I don’t think it’s much of a leap to then presume that all respiratory viruses could do this, whether endemic, zoonotic, or capable of causing mild, severe, or no overt disease at all.

*Imported Post

1. This post from 04AUG2013 was posted over on my old blog platform virologydownunder.blogspot.com.au. It has now been moved here and lightly edited for formatting, grammar and typos.