Infection patterns of endemic human coronaviruses in rural households in coastal Kenya

Abstract

Background: The natural history and transmission patterns of endemic human coronaviruses are of increased interest following the emergence of severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2). Methods: In rural Kenya 483 individuals from 47 households were followed for six months (2009-10) with nasopharyngeal swabs collected twice weekly regardless of symptoms. A total of 16,918 swabs were tested for human coronavirus (hCoV) OC43, NL63 and 229E and other respiratory viruses using polymerase chain reaction. Results: From 346 (71.6%) household members, 629 hCoV infection episodes were defined, with 36.3% being symptomatic: varying by hCoV type and decreasing with age. Symptomatic episodes (aHR=0.6 (95% CI:0.5-0.8) or those with elevated peak viral load (medium aHR=0.4 (0.3-0.6); high aHR=0.31 (0.2-0.4)) had longer viral shedding compared to their respective counterparts. Homologous reinfections were observed in 99 (19.9%) of 497 first infections. School-age children (55%) were the most common index cases with those having medium (aOR=5.3 (2.3 – 12.0)) or high (8.1 (2.9 - 22.5)) peak viral load most often generating secondary cases. Conclusion: Household coronavirus infection was common, frequently asymptomatic and mostly introduced by school-age children. Secondary transmission was influenced by viral load of index cases. Homologous-type reinfection was common. These data may be insightful for SARS-CoV-2.

Origins and Evolution of Seasonal Human Coronaviruses

“…Our results demonstrate that recombination frequently occurs beyond the spike protein which is often the focus of recombination analyses. As viral co-infections are frequently identified in patients [ 3 , 10 ], recombination between sHCoV species could be a real-world phenomenon that needs to be considered in studying the evolution of human CoVs in the SARS-CoV-2 era. To what extent do these within and between sHCoV species recombination events facilitate the expansion of sHCoV variants and, thereby, the fitness of these sHCoVs warrants further investigation.…”

“…CoV infections primarily involve the upper respiratory tract and the gastrointestinal tract, mostly producing mild respiratory diseases, but may sometimes cause life-threatening bronchiolitis and pneumonia in infants, young children, elderly, and immunocompromised individuals [ 2 , 3 , 4 ]. While the sHCoVs are globally distributed with a general seasonality between December and April, the frequency of detection varies by location and time [ 5 , 6 , 7 , 8 , 9 , 10 , 11 ]. Differences in clinical presentation and frequencies of detection by age and patient groups have been observed between the sHCoV infections and might be immune-mediated [ 1 , 11 , 12 , 13 ].…”

How immunity from and interaction with seasonal coronaviruses can shape SARS-CoV-2 epidemiology

“…Our estimates for the duration of homotypic protection following HCoV infection are comparable with other estimates, such as a cohort study where 8/216 (3%) confirmed infected individuals were reinfected over 5 y, and the median reinfection time in a study of 10 individuals ( 32 ) varied between 30 and 55 mo, depending on strain. However, estimates vary, with a larger study in Michigan estimating mean strain-specific reinfection to be between 19 and 33 mo ( 33 ), 19.9% of first infections being reinfected within 6 mo in Kenya ( 34 ), and a historical study, of just one seasonal HCoV strain (229E), estimating the time until T cells could no longer neutralize new strains at 8 y to 17 y ( 24 ). Other coronaviruses can also give indications on the duration of immunity, with T cells to SARS-CoV-1 detectable up to 11 y postinfection ( 35 ).…”

Origins and Evolution of Seasonal Human Coronaviruses

“…However, recombination between sHCoV species was only observed between species in the same genus, i.e., between 229E and NL63 and between HKU1 and OC43, and was only identified in the spike and WGS datasets. Because sHCoV co-infections are frequently identified in community and patient isolates [3, 10], recombination within and between sHCoV species might be a frequent occurrence and could increase the breadth of the sHCoV species’ variants.…”

“…It was estimated for the spike and WGS that there was a 61% and 35% probability, respectively, that the camelid CoVs arose from the sHCoV 229E. Taken together, there is a high degree of uncertainty as to OC43 WGS Bovine [36] Murine [34] Rabbit [10] Canine [9] Spike Bovine [35] Murine [19] Camel [14] Rabbit [14] Canine [8] Equine [5] Nucleocapsid Porcine [25] Bovine [23] Murine [18] Rabbit [15] Equine [10] Membrane Camel [75] Murine [6] Rabbit [3] Porcine [3] Equine [2] Bovine [2] Bat [2] Envelope Murine [30] Porcine [24] Bovine [20] Equine [8] Rabbit [6] Camel [3] The zoonotic origins of the sHCoVs NL63 and HKU1 were inferred to be bat and murine CoVs, respectively, with no apparent intermediate hosts (Figure 2 and Table 1). The two HKU1 A and B genotypes formed distinct and well-supported clades, with very long branch lengths, in all the MCC trees derived from the four structural proteins (Figure 2).…”