Rhinoviruses (RVs)...a primer

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Wheezing after respiratory virus infection...

Takeyama and colleagues from Japan delved into the viruses present among young children (≤ 3-years of age) hospitalized with a clinically defined lower respiratory tract infection.

This exemplifies what many such studies do; sample from the upper respiratory tract to find signs of replicating virus in order to study a disease of the lower respiratory tract. 

It's a stretch but if you go along with it you are implying that an upper respiratory tract infection either triggers the symptoms from afar or that the virus travels into the lower respiratory tract to directly cause inflammation and/or cell destruction.

Viruses were detected by PCR-based methods.

Some key findings...

• Respiratory syncytial virus (RSV) was the virus detected most often (51/102 samples from 153 children) in children who were admitted with wheezing followed by rhinoviruses (RV; 21 or 14%), RSV+RV (12 or 8%) and then parainfluenza virus 3 (PIV3; 8 or 5%), influenza virus (IFV; 5 or 3%) or human metapneumovirus (hMPV; 5 or 3%)
• A similar pattern was observed in 259 children who were admitted without wheezing (RSV-25%; RV 9%; IFV 7%; RSV+RV-4%; PIV3-3%; hMPV-1%)
• 67% of children with wheezing were virus positive (POS)
• Children with an allergic predisposition (IgE antibody levels >30IU/mL at admission and a parental history of asthma) POS for RSV more often had wheezing later
• Children who were wheezing & RV POS when they were admitted were more likely to wheeze again than were those who were RV POS without wheeze at admission.

So [allergic predisposition + RSV] or [wheeze/clinical severity + RV] were 2 factors related to subsequent wheeze.

The authors also raised the spectre of RV positivity occurring in asymptomatic individuals in other studies. However, that can happen to some extent with all respiratory viruses. No other virus has 160 distinct type like the RVs...but that's another story.

Article...

1. http://www.ncbi.nlm.nih.gov/pubmed/24535712

Little rhino...

To the tune of ‘I’m a little teapot’

I’m a little rhino,

Strain in doubt

Bind with my canyon

Bind without

When I’ve replicated

Just the right amount

You’ll need to get a tissue to blow me out

[alternate: exacerbate your wheezing and cough me out]

Thanks to Cassandra Faux for putting this one together back in 2007.

Randall the red-nosed toddler...

To the tune of Rudolph the red-nosed reindeer

Randall the red-nosed toddler
Had a very runny nose 
Asthma exacerbation 
Fever adding to his woes 

All of the other toddlers 
Didn't have immunity 
They all came down with symptoms 
Differing in severity 

Then one group of researchers 
Virus-hunting was their game 
Swabbed, extracted, amplified
A rhino POS of course was spied 

Randall’s rhino was sequenced 
Turned out to be rhino C
Randall the red-nosed toddler
Just a 'common' cold indeed!

Randall the red-nosed toddler

Had a very runny nose 
Asthma exacerbation 
Fever adding to his woes 


Thanks to Katherine Arden and Cassandra Faux for helping me put these together back in 2008.

Happy Birthday rhinoviruses (RVs) - 60 years old today!

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A drug to stop rhinovirus (HRV) infections in patients with chronic obstructive pulmonary disease (COPD)?

For those who don't know, the HRVs are the most frequent infecting agents (that we know of) of the human upper (and perhaps lower but that work is not done) respiratory tract (URT).The first HRV was isolated in 1953 in the UK and the viruses were soon burdened by the label "common cold viruses". This was largely because early studies were conducted in adults who generally have milder outcomes.
There are about 77 genetically distinct HRV-As, 60 HRV-Cs and 30 HRV-Bs - that's nearly 170 distinct viruses (includes serotypes and genotypes)! Imagine 170 distinct coronaviruses.

In the past they were classified by the type of cell they infected/receptor they used into major (most of them used ICAM-I as the receptor) and minor (the rest; use VLDL-R as the receptor) groups. Sequencing is the preferred method to classify them today.

The receptor for the HRV-Cs remains unknown and they do not grow in routine cell lines instead needing more advanced culture methods. Because of this, studies predating 1988 (the first published PCR primers) generally don't account for the HRV-Cs, even though they were there and causing infections.

A.Prof Eva Kathryn Miller and I recently reviewed the HRV-Cs in some detail. Around 70 distinct HRV genotypes can circulate at a single place over a year...depending on the population being studied. I and others have found that to be the case in both the community and in hospital-based populations.

A recent article from Yamaya and colleagues suggests that a mucolytic drug (stimulates surfactant production and release to help the airways clear themselves of gunk) might be of use in treating HRV infections in COPD patients at least.

Exacerbations, which are mostly due to viruses, are the main contributor to disease burden in patients suffering from COPD, as they are in those with asthma.

The drug, ambroxol hydrochloride is already thought to reduce the frequency of URT disease and may reduce ICAM-I expression. The authors tested this using a major group HRV, HRV-B14 and found reduced release of virus, ICAM-I levels and reduced viral RNA levels.

Prophylactic use may inhibit HRV-B14 infection and modulate the inflammatory response to infection. Many of the differences were moderate (mostly arithmetic rather than logarithmic), albeit statistically significant.

It would be interesting to see what effect the drug has on other major group HRVs, minor group HRVs and on the hard to culture HRV-Cs.

Editor's Note #6.

I've finally started to rebuild the rhinovirus (HRV) page. For someone whose main interest is these little dudes...well, it was in a pretty woeful state. How embarrassment. Expect to see it take shape over the coming weeks.