Table 1 Recent epidemiological papers on respiratory infections and co-infections
PAPER | VIRUSES ANALYSED (detection methods) | POPULATION | CONCLUSIONS | ||||||||||||||||
|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|
Flu | HRV | HEV | HPeV | PIV | hMPV | ADV | RSV | Coronavirus | HBoV | Polyomavirus | Â | Â | |||||||
H1N1 | A | B | Â | Â | Â | Â | Â | Â | Â | HCoV 229E | HCoV OC43 | HCoV NL63 | HCoV HKU1 | Â | WUPyV | KIPyV | Â | Â | |
Greensill, 2003 | Â | Â | Â | Â | Â | Â | Â | X(a) | Â | X(a) | Â | Â | Â | Â | Â | Â | Â | pediatric (30, ventilated and with bronchiolitis) | 70% rates of co-infection RSV-hMPV in a cohort of infants with bronchiolitis, suggesting that dual infection may predispose for a more severe disease. |
Viazov, 2003 |  |  |  |  |  |  |  | X(a) |  | (d) |  |  |  |  |  |  |  | children <2 years (63) with RTD | 17,5% hMPV positive, 23% RSV positive, 4.7% hMPV-RSV coinfections. Similar symptoms between hMPV+ and RSV+ children. |
Esper, 2004 |  |  |  |  |  |  |  | X(a) |  |  |  |  |  |  |  |  |  | children <5 years (688) negative for RSV, PIV, Flu A and B, ADV | 8% hMPV positive samples |
Xepapadaki, 2004 | Â | X(a) | X(a) | X(a) | Â | Â | X(a) | X(a) | X(a) | X(a) | X(a) | X(a) | X(a) | X(a) | Â | Â | Â | pediatric (56) with acute bronchiolitis | 16% bronchiolitis is hMPV positive, 67.9% RSV positive, without clinical d(d)ference. |
Konig, 2004 | Â | Â | Â | Â | Â | Â | Â | X(a) | Â | X(a) | Â | Â | Â | Â | Â | Â | Â | children requiring intensive support (85) | coinfections with RSV and hMPV are more severe than infections with either RSV or hMPV alone in young children |
Semple, 2005 | Â | Â | Â | Â | Â | Â | Â | X(a) | Â | X(a) | Â | Â | Â | Â | Â | Â | Â | <2-year-old infants with bronchiolitis(196) | hMPV and RSV co-infection is associated with increased disease severity |
van Woensel, 2006 |  |  |  |  |  |  |  | X(b) |  | X(b) |  |  |  |  |  |  |  | pediatric (30, mean age 10 weeks, ventilated and with bronchiolitis) | No virus co-infection between RSV and hMPV in a cohort of infants with bronchiolitis |
Foulongne, 2006 |  | (d) | (d) |  |  |  | (d) | X(a) | (d) | (d) |  |  |  |  |  |  |  | 589 children hospitalized with respiratory disease<5 years | 8.5% rates of hMPV infections, the second leading cause of RTD after RSV, 30% of the cases are hMPV-RSV coinfections. The duration of hospitalization and requirement for supplemental oxygen were increased in case of hMPV-RSV coinfections |
Lazar, 2004 | Â | Â | Â | Â | Â | Â | Â | X(a) | Â | X(a) | Â | Â | Â | Â | Â | Â | Â | 46 children with mild to severe RSV disease (PIV, fluA and B, ADVnegative) | hMPV did not contribute to the severity of RSV disease |
Canducci, 2008 | Â | Â | Â | Â | Â | Â | Â | X(a) | Â | X(a) | X(a) | X(a) | X(a) | X(a) | X(a) | Â | Â | 322 infant patients with acute respiratory disease | RSV-hMPVs co-infections were observed in less severe respiratory disease when compared to RSV mono-infections |
Chiu, 2005 | Â | (d) | (d) | Â | Â | Â | (d) | X(a) | (d) | (d) | X(a) | X(a) | X(b) | Â | Â | Â | Â | hospitalized with fever and acute respiratory symptoms (587) | 4.4% HCoV infections. HCoV-NL63 can present as croup, asthma exacerbation, febrile seizures, and high fever. |
van der Hoek,2006 |  | X(a) | X(a) |  |  |  | X(a) |  |  | X(a) |  |  | X(b) |  |  |  |  | children<3 years with LRTIs (940) | HCoV-NL63 RNA was detected in 5.2% of cases;43% of the HCoV-NL63-positive patients with high viral load and absence of co-infection suffered from croup. Most co-infections were with RSV-A HCoV-NL63 co-infection with RSV-A occurred mainly in hospitalised patients in contrast to HCoV-NL63 co-infections with PIV3 that were exclusively present in the outpatient group. Lower HCoV-NL63 viral load in patients coinfected with RSV or PIV3 than in patients infected with HCoV-NL63 alone |
Dare, 2007 | Â | Â | Â | Â | Â | Â | Â | Â | Â | Â | X(b) | X(b) | X(b) | X(b) | Â | Â | Â | 1156 patients with pneumonia, 513 outpatients, 281 controls | 1.8% of patients with pneumonia, 2.3% of outpatients and 2.1% of controls had HCoV infections. In control patients, infection with any HCoV type or with all types combined was not associated with pneumonia |
Kuypers, 2007 |  | X(a) |  |  |  |  | X(a) | X(a) | X(a) | X(a) | X(b) | X(b) | X(b) | X(b) |  |  |  | 1043 pediatric (0–19 years old) respiratory specimens | CoVs were detected in 6.3% of specimens. 45.5% CoV-positive specimens also had another respiratory virus detected, most commonly RSV (67%). CoV subtypes NL63 and HKU1 accounted for the majority of CoVs detected. |
Minosse, 2008 |  |  |  | X(a) |  |  |  |  | X(a) |  |  |  | X(a) |  |  |  |  | hospitalized adult patients (433, mean age 56 years) | 2% Hcov NL63 positive, 33% coinfected NL63-HRV, 10% coinfected NL63-ADV |
Wu, 2008 |  |  |  |  |  |  |  | X | X | X |  |  | X(b) |  |  |  |  | 539 children < 15 years with respiratory disease | 1.3% HCoV NL63 positive, 43% of HCoV infection are coinfections (RSV, ADV, hMPV) |
Gaunt, 2010 | Â | X(b) | X(b) | Â | Â | Â | X(b) | Â | X(b) | X(b) | X(b) | X(b) | X(b) | X(b) | Â | Â | Â | 11661 respiratory samples | high rate of coinfections observed for HKU1, NL63 and OC43, mostly with RSV. No d(d)ferences of HCoV viral load were observed between single infection and RSV coinfection. Detection of CoVs should not be interpreted as representing an incidental infection without contribute to disease. |
Choi, 2006 |  | X(a) and (d) | X(a) and (d) | X(a) |  |  | X(a) and (d) | X(a) | X(a) and (d) | X(a) and (d) | X(a) | X(a) | X(a) |  | X(a) |  |  | 515 children< 5 years old with LRTIs | The prevalence of HboV was the second (11%), the first was RSV (23%). Among HBoV infections, a high rate (38%) was coinfection. |
Allander, 2007 |  | X(b), (c), (d), (e) | X(b), (c), (d), (e) | (c), (e), X(a) | (c), (e), X(a) |  | X(b), (c), (d), (e) | (c), X(a) | X(b), (d), (e) | (c), (d), (e), X(a) | X(a) | X(a) | X(b), (e) | X(b), (e) | X(b), (e) |  |  | 259 children (median age, 1.6 years) who had been hospitalized for acute expiratory wheezing | Acute HBoV infections appears associated with presence of viral DNA in the blood as the HBoV DNA was reported more prevalent in the patients blood during the acute symptoms than after recovery. High load and viremic HBoV infection were associated with respiratory tract symptoms, while detection of a low viral load in the nasopharinx alone has uncertain relevance |
Christensen, 2008 | Â | X(b) | X(b) | X(b) | X(b) | Â | X(b) | X(b) | X(b) | X(b) | X(b) | X(b) | X(b) | Â | X(b) | Â | Â | Â | HBoV was detected in 12% of samples. It was the fourth most common virus in the material after RSV (25%), HRV (17%) and hMPV(14%). Multiple viral infections were common and were present in 78% of the samples, more commonly RSV |
Dina, 2009 |  | X(a) | X(a) | X(a) |  |  | X(a) | X(a) | (d), (c), X(b), x(a) |  |  |  |  |  | X(b), X(a) |  |  | 842 patients hospitalized with respiratory symptoms (mean age 22 years) | The prevalence of HBoV infection was 3.8%. HBoV. Viral load appears to be linked to the severity of the disease. |
Wang, 2010 | Â | X(a) | X(a) | X(a) | Â | Â | X(a) | X(a) | X(a) | X(a) | X(a) | X(a) | X(a) | X(a) | X(a),X(b), (e) | Â | Â | 817 children with respiratory tract infection | HBoV was ident(d)ied in 12% of samples. Co-infection rate with other respiratory viruses was 51%. HBoV was found frequently in children with respiratory tract symptoms associated with other viruses, and persisted in the respiratory tract, in serum and urine. The presence of IgM was significantly more prevalent in viremic patients and those diagnosed with high load of HBoV DNAin nasal/throat swabs |
Don, 2010 |  | (e) | (e) |  |  |  | (e) | (e) | (e) | (e) |  |  |  |  | (e) |  |  | 124 children with presumptive pneumonia<15 years | Mixed infections were found in 25% of cases. Serological evidence of acute HBoV infection was found in 12% of children with pneumonia and in more than half of cases with single HBoV infection.This suggests that HBoV may be a fairly common cause of pneumonia in children |
Soderlund-Venermo, 2009 |  | X(a) | X(a) | X(a) | X(a) |  | X(a) | X(a) | X(a) | X(a) | X(a) | X(a) | X(a) | X(a) | X(a), (e), X (b) |  |  | 259 weezing children <15 years, 115 healthy adults | Serologically confirmed primary HBoV infections detected in symptomatic children with no signs of other respiratory virus infections demonstrate that HBoV is a cause of acute wheezing in young children. Accurate HBoV diagnosis requires serologic analysis or PCR of serum, PCR of NPAs alone is insufficient. HBoV is the most probable cause of respiratory tract disease (d) the patients has single infection, a high viral load in NPA nasopharyngeal aspirates and viremia |
Martin, 2010 | Â | X(a) | X(a) | X(a) | Â | Â | X(a) | X(a) | X(a) | X(a) | X(a) | X(a) | X(a) | X(a) | X(b) | Â | Â | 119 children attending daycare | 28% tested positive for HBoV. HBoV was detected significantly more often than any of the 14 respiratory viruses but HRVs. HboV DNA can persist for several months in the respiratory tract |
Jin, 2012 |  | X(a) | X(a) | X(a) |  |  | X(a) | X(a) | X(a) | X(a) |  |  | X(a) | X(a) | X(a) |  |  | 813 children<14 years with acute lower respiratory tract infections | The most frequently detected virus was RSV (40.%), followed by HRV (20%), HBoV (11.5%), PIV1-3 (8%), AdV (7.5%), FluA (7%), HMPV (6.%), NL63 (4%), HKU1 (2.%) and FluB (0.98%). Of the HCoV-HKU1 and HCoV-NL63-positive samples, 74% were co-infected with at least another virus, most commonly HRV and RSV. |
Esposito, 2012 | Â | X(a) | X(a) | X(b) | X(b) | Â | X(a) | X(a) | X(a) | X(a) | X(a) | X(a) | X(a) | X(a) | X(a) | Â | Â | 592 children with radiographically confirmed pneumonia | HBoV was the most frequently detected virus(10%) after RSV (31%) and HRV (24%) |
Le, 2007 |  | X(a) | X(a) | X(a) |  |  | X(a) | X(a) | X(a) |  | X(a) | X(a) | X(a) | X(a) |  | X(b) |  | 2,263 samples from children <4 years of age and 374 from children >4 years of age for routine respiratory virus detection | 2.7% samples positive for WU polyomavirus and 71% coinfected with other viruses. WU polyomavirus was the sole virus detected in 20 specimens from patients with respiratory illness, which suggests that it may be a respiratory pathogen. Repeated identification of WU polyomavirus in the same patients suggests that it may persistently infect humans |
Han, 2007 |  | X(a) | X(a) | X(a) |  |  | X(a) | X(a) | X(a) | X(a) | X(a) | X(a) | X(a) | X(a) | X(a) | X(a) |  | 486 children with acute lower respiratory tract, 72 asymptomatic children<6 years | WUPyV was detected in 7% children with LARD, 4.2% of asymptomatic children and as coinfection with other respiratory viruses in 67.6%. Although WUPyV was frequently detected, its clinical role has not been distinguished from that of coinfecting viruses |
Bialasiewicz, 2008 |  | X(a) | X(a) | X(a) |  |  | X(a) | X(a) | X(a) | X(a) | X(a) | X(a) | X(a) | X(a) | X(b) | X(b) | X(b) | 2866 respiratory sample from people with acute respiratory diseases (mean age 9.2 years) | KIV and WUV were found at a prevalence of 2.6% and 4.5%, respectively. Level of co-infection of KIV or WUV with other viruses was 74.7% and 79.7%, respectively. It is not possible to prove a causal relationship between the detection of KIV and WUV and respiratory disease from these findings |
Neske, 2008 | Â | (d) | (d) | Â | Â | Â | (d) | Â | (d) | Â | Â | Â | Â | Â | X(a) | X(a) | Â | 1,326 hospitalized children with acute respiratory diseases | 4.9% positive WUPyV. 56% were co-infections with other viruses (ADV, fluA, hBoV and RSV). |
Babakir-Mina, 2010 |  |  |  |  |  |  |  |  |  |  |  |  |  |  |  | X(b) | X(b) | 153 HIV-1-infected patients (mean age 42 years), 130 controls | 2.6% KIPyV positive and 4.6% WUPyV positive among HIV-1–infected patients compared with 3.1% KIPyV positive and 0,8% WUPyV positive in blood donors. No association found between CD4+ cell counts in HIV-1 positive patients and infection with KIPyV or WUPyV |
Debiaggi, 2010 |  | X(a) | X(a) | X(a) |  |  | X(a) | X(a) | X(a) | X(a) | X(a) | X(a) | X(a) | X(a) | X(a) | X(a) | X(a) | 31 asymptomatic adulthematopoietic stem cell transplant recipients;486 children with acute respiratory disease< 2 years | 0.79% KIPyV, 0.79% WuPyV positive among transplant recipients; 1.4% KIPyV and 0.2% WUPyV in children. WU/KIPyVs have a low pathogenic potential in young children. Brief and asymptomatic infection can occur in hematopoietic transplant recipients. |
Zhuang, 2011 | Â | X(b) | X(b) | X(b) | Â | Â | X(b) | X(b) | X(b) | X(b) | Â | Â | Â | Â | X(b) | X(a) | Â | 771 children with acute respiratory tract infection and 82 samples from healthy subjects | In most of infected children single WUPyV infection was detected.It suggests that the newly described polyomavirus can cause acute respiratory tract infection |
Rao, 2011 | Â | X(a) | X(a) | X(a) | Â | Â | X(a) | X(a) | X(a) | X(a) | X(a) | X(a) | X(a) | X(a) | Â | X(b) | X(b) | pediatric hematology or oncology patients and immunocompetent controls with acute respiratory illnesses | Prevalence of WUPyV and KIPyV is similar in hematology/oncology patients (3% and 5.6%, respectively) compared with the general pediatric population (5%and 2.3, respectively). High co-detection rates with other viruses (RSV and HRV) in both groups. Higher viral loads for KIPyV (but not for WUPyV) in the immunocompromised group was detected and infection with either virus occurred in older children compared with controls, which may suggest viral-reactivation |
Lau, 2007 | Â | (d) | (d) | X(a) | Â | Â | (d) | X(a) | (d) | (d) | X(a) | X(a) | X(a) | X(a) | Â | Â | Â | 203 nasopharyngeal aspirates (NPAs), negative for common respiratory viruses from hospitalized children | HRV-C is an important cause of febrile wheeze and asthmatic exacerbations in children requiring hospitalization. No clear clinical difference has been noted between single or mixed HRV-C infections |
Harvala, 2008 |  | X(a) | X(a) |  |  | X(a) | X(a) | X(a) | X(a) | X(a) |  |  |  |  | X(a) |  |  | 4,173 respiratory samples for routine respiratory virus detection | High rate of coinfections, ow frequency of detection and lack of clear disease associations indicate that HPeV1 and −6 are not major pathogens in individuals presenting with respiratory disease |
Jin, 2009 |  | X(a) | X(a) | X(a) |  |  | X(a) | X(a) | X(a) | X(a) | X(a) | X(a) | X(a) | X(a) | X(a) |  |  | 406 children< 14 years with RTI | 13% HRV positive (22% HRV-A, 12% HRV-B, 19% HRV-C). Monoinfection was observed in more than half of cases, HRV-C is an important cause of RTIs in children. Patients infected with HRV-C may exhibit different clinical features from patients infected with HRV-A/B |
Miller, 2009 |  |  |  | X(a) |  |  |  |  |  |  |  |  |  |  |  |  |  | 1052 hospitalized children< 5 years with acute respiratory illness | HRVCs were detected in 7% of children hospitalized for fever or respiratory conditions and constituted almost half of all HRVs-associated hospitalizations, suggesting that this novel group causes a substantial burden of pediatric disease |
Yozwiak, 2010 |  |  |  |  | X(a) |  |  |  |  |  |  |  |  |  |  |  |  | 3,800 children aged 2 to 13 years with respiratory illness | EV109 isolates were then detected in 1.6% of respiratory samples of children with influenza like illness (ILI) and recognized to have a pathogenetic role in the illness |
Debiaggi, 2012 | Â | X(a) | X(a) | X(a) | X(a) | Â | X(a) | X(a) | X(a) | X(a) | X(a) | X(a) | X(a) | X(a) | X(a) | X(a) | X(a) | 1149 nasopharingeal aspirates | HEV109 infection may be associated to ARDs both in infants and in hematopoietic stem cell transplantation recipients |
Piralla, 2012 | Â | X(a) | X(a) | X(a) | X(a) | X(b) | X(a) | X(a) | X(a) | X(a) | X(a) | X(a) | X(a) | X(a) | X(a) | X(a) | X(a) | 3,525 patients with respiratory syndrome | The prevalence of HpeV is 0.4%. The most commonly identified HPeVs were HpeV1(58%) and HpeV3 (37%). Although not circulating at high frequency and unlikely to cause respiratory syndrome, HPeV was associated with severe clinical syndromes in a minority of newborns. The frequent association of HPeV with other respiratory viruses may indicate a less pathogenic role for HPeV compared to the other viruses |
Renois, 2010 | X(a) | X(a) and X(b) | X(a) | X(a) | X(a) | Â | X(a) | X(a) | X(a) | X(a) | X(a) | Â | Â | Â | X(a) | Â | Â | 56 adults and 39 children visited for influenza-like illnesses | 31% of H1N1 infections, 16% coinfected with HRV (60%) and RSV, CoV229E, HBoV (20%). No difference in disease severity between single and mixed infections |
Casalegno, 2010 | X(b) |  |  | X(b) |  |  |  |  |  |  |  |  |  |  |  |  |  | pediatric (2121, mean age 3.8 years) | The presence of HRV reduce the risk of H1N1 infection. |
Schnepf, 2011 | X(b) | X(a) | X(a) | X(a) | Â | Â | X(a) | X(a) | X(a) | X(a) | X(a) | X(a) | X(a) | Â | Â | Â | Â | in adult and paediatric patients with Influenza-like illness (413) | 16% of H1N1 infections, 19% of them were co-infections (mainly HRV). Among 50% of non-H1N1 infections were HRV infections and increase of H1N1 cases was associated with rapid HRV infection decline |