Background Rhinoviruses (RVs) are ubiquitous pathogens and the principal etiological agents of common cold. Despite the high frequency of RV infections, data describing their long-term epidemiological patterns in a defined population remain limited. Methods Here, we analysed 1,070 VP4/VP2 genomic region sequences sampled at Kilifi County Hospital on the Kenya Coast. The samples were collected between 2007 and 2018 from hospitalised paediatric patients (< 60 months) with acute respiratory illness. Results Of 7,231 children enrolled, RV was detected in 1,497 (20.7%) and VP4/VP2 sequences were recovered from 1,070 samples (71.5%). A total of 144 different RV types were identified (67 Rhinovirus A, 18 Rhinovirus B and 59 Rhinovirus C) and at any month, several types co-circulated with alternating predominance. Within types multiple genetically divergent variants were observed. Ongoing RV infections through time appeared to be a combination of (i) persistent types (observed up to seven consecutive months), (ii) reintroduced genetically distinct variants and (iii) new invasions (average of eight new types, annually). Conclusion Sustained RV presence in the Kilifi community is mainly due to frequent invasion by new types and variants rather than continuous transmission of locally established types/variants.

IntroductionOver 24 million people have been infected globally with the novel coronavirus, SARS-CoV-2, with more than 820,000 succumbing to the resulting COVID-19 disease as of the end of August 2020. The molecular mechanisms underlying the pathogenesis of the disease are not completely elucidated. Thus, we aim to understand host response to SARS-CoV-2 infection by comparing samples collected from two distinct compartments (infection site and blood), obtained from COVID-19 subjects and healthy controls.MethodsWe used two publicly available gene expression datasets generated via RNA sequencing in two different samples; nasopharyngeal swabs and peripheral blood mononuclear cells (PBMCs). We performed a differential gene expression analysis between COVID-19 subjects and healthy controls in the two datasets and then functionally profiled their differentially expressed genes (DEGs). The genes involved in innate immunity were also determined.ResultsWe found a clear difference in the host response to SARS-CoV-2 infection between the two sample groups. In COVID-19 subjects, the nasopharyngeal sample group indicated upregulation of genes involved in cytokine activity and interferon signalling pathway, as well as downregulation of genes involved in oxidative phosphorylation and viral transcription. Host response in COVID-19 subjects for the PBMC group, involved upregulation of genes involved in the complement system and immunoglobulin mediated immune response. CXCL13, GABRE, IFITM3 were upregulated and HSPA1B was downregulated in COVID-19 subjects in both sample groups.ConclusionOur results indicate the host response to SARS-CoV-2 is compartmentalized and suggests potential biomarkers of response to SARS-CoV-2 infection.HighlightsTranscriptomic profiling from publicly available RNA-seq count data revealed a site-specific immune response in COVID-19.Host response was found cellular-mediated in nasopharyngeal samples and humoral-mediated in PBMCs samples.CXCL13, GABRE and IFITM3 commonly upregulated and HSPA1B downregulated in both sample groups highlights the potential of these molecules as markers of response to SARS-CoV-2 infection.

Background: Human rhinovirus (HRV) is an ubiquitous pathogen and the principal etiologic agent of common cold. Despite the high frequency of HRV infections, data describing its long-term epidemiological patterns in a single population remain limited. Methods: We analysed 1,070 VP4/VP2 genomic region sequences obtained from samples collected between 2007-2018 from hospitalised paediatric patients (< 60 months) with acute respiratory disease in Kilifi County Hospital on the Kenya Coast. Results: Of 7,231 children enrolled, HRV was detected in 1,497 (20.7%) andVP4/VP2 sequences were recovered from 1,070 samples (71.5%). A total of 144 different HRV types were identified (67 HRV-A, 18 HRV-B and 59 HRV-C) and at any time-point, several types co-circulated with alternating predominance. Within types multiple genetically divergent variants were observed. Ongoing HRV infections appeared to be a combination of (i) persistent types (observed up to seven consecutive months), (ii) reintroduced genetically distinct variants and (iii) new invasions (average of 8 new types, annually). Conclusion: Sustained HRV presence in the Kilifi community is mainly due to frequent invasion by new types and variants rather than prolonged circulation of locally established strains.