Interpretation of results and comparison with previous findings
In our study, the effect of age on the respiratory virus-specific IgG
levels varied between RSV and RV and between children and adults,
indicating, for the first time, different patterns of virus specific
immune responses over the course of life. Regarding RV, our results
indicate that IgG levels were higher (RV-B) or remained stable (RV-A and
-C) over time during childhood, and were lower with age from
adolescents/early adulthood, while RSV IgG levels seemed to increase
with age both in childhood and in adulthood. Previous studies in the
literature were restricted to children and led to contradictory results
regarding the effect of age on RV-specific IgG responses, with studies
showing a negative association (14), a positive association (22) or no
association (23). These studies were based on relatively small sample
sizes (range: 120-300) and were often based on PCR data which do not
allow to draw conclusion regarding immune responses in the studied
populations thus limiting the comparability between studies. To the best
of our knowledge, there are no study investigating the associations
between RSV and RV-specific immune response among adults.
Regarding sex, our results showing higher RV-specific IgG levels in
women than in men confirm the existing knowledge reporting higher innate
and adaptative immune response in women than in men for various viruses
(24–26). Further studies are needed to identify the respective effects
of hormones, of gender differences in environmental exposures and
lifestyle factors and of genetic factors in the sex-specific immune
responses.
Our results suggest that higher BMI was associated with lower levels of
RV-specific IgG in both children and adults, which is in line with
previous observations. It is well known that obesity is a risk factor
for chronic diseases, and it seems to be often linked to impaired
immunity (27). Indeed, in obese children and adults, excessive mass of
adipose tissues impairs proper development and activity of immune cells
(28), possibly through an anti-inflammatory mechanism (29). However, no
clear connection between obesity and antibody response to respiratory
viruses is establish.
Regarding smoking, our results did not provide evidence for an effect of
passive smoking on RV- and RSV-specific IgG levels among children, but
in adults, former smoking, and to a greater extent current smoking
status had higher IgG levels against RSV and all RV species. Similarly
to our results, one study performed among 217 children from birth to one
year of age did not find any association between RSV IgG level and
passive smoke/smoking during pregnancy (10). Among adults, a former
study did not report any association between tobacco smoking and RSV
immune responses, assessed by complement fixation test (11). More
recently, a study performed among 245 adults, including two third of
HIV+ patients, identified a positive association between current smoking
and RSV specific IgG, independently from HIV status (12). Interestingly,
a positive effect of smoking on respiratory-virus specific IgG responses
is supported by in vitro studies that demonstrated that ICAM1, a
major epithelial airway receptor for RV in both large and small airways,
is upregulated in smokers, resulting in an increased vulnerability of
smokers to RV infections (30,31). Furthermore, tobacco smoke and RV
infection may impair the barrier function of respiratory epithelium
(32).
RSV and RV can be detected throughout the year, but highest prevalence
and most of illness related to these viruses occur during winter
(18,33,34). Accordingly, in our study we observed higher levels of RSV
specific IgG in all seasons as compared with summer in adults. Until
now, several studies investigated the effect of the season of birth on
RSV specific IgG responses in young children (10,35) but, no study
focused on the season of blood sampling and respiratory virus-specific
IgG responses. This seasonal variations of immune response while the
virus is present throughout the year may be attributable to climate
factors, with lower temperatures and higher relative humidity being
correlated with higher RV and RSV incidences as observed for SARS-Cov-2
(36–39).