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3. Spread and evolution of respiratory syncytial virus A genotype ON1, Coastal Kenya, 2010-2015

Author

Otieno, James R., Kamau, Everlyn M., Agoti, Charles N., Lewa, Clement, Otieno, Grieven, Bett, Ann, Ngama, Mwanajuma, Cane, Patricia A., and Nokes, D. James

Subjects
Pneumonia -- Genetic aspects -- Analysis, Amino acids -- Analysis, Health
Abstract

Respiratory syncytial virus (RSV) is a major cause of pneumonia and bronchiolitis among infants and children globally (1,2). Although immune responses develop in those who have had RSV infection during [...]

Published
2017
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9. Nucleoside Reverse Transcriptase Inhibitor Resistance Mutations Associated with First-Line Stavudine-Containing Antiretroviral Therapy: Programmatic Implications for Countries Phasing Out Stavudine

Author

Tang, Michele W., Rhee, Soo-Yon, Bertagnolio, Silvia, Ford, Nathan, Holmes, Susan, Sigaloff, Kim C., Hamers, Raph L., de Wit, Tobias F. Rinke, Fleury, Herve J., Kanki, Phyllis J., Ruxrungtham, Kiat, Hawkins, Claudia A., Wallis, Carole L., Stevens, Wendy, van Zyl, Gert U., Manosuthi, Weerawat, Hosseinipour, Mina C., Ngo-Giang-Huong, Nicole, Belec, Laurent, Peeters, Martine, Aghokeng, Avelin, Bunupuradah, Torsak, Burda, Sherri, Cane, Patricia, Cappelli, Giulia, Charpentier, Charlotte, Dagnra, Anoumou Y., Deshpande, Alaka K., El-Katib, Ziad, Eshleman, Susan H., Fokam, Joseph, Gody, Jean-Chrysostome, Katzenstein, David, Koyalta, Donato D., Kumwenda, Johnstone J., Lallemant, Marc, Lynen, Lutgarde, Marconi, Vincent C., Margot, Nicolas A., Moussa, Sandrine, Ndung'u, Thumbi, Nyambi, Phillipe N., Orrell, Catherine, Schapiro, Jonathan M., Schuurman, Rob, Sirivichayakul, Sunee, Smith, Davey, Zolfo, Maria, Jordan, Michael R., and Shafer, Robert W.

Published
2013
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11. Recent trends and patterns in HIV‐1 transmitted drug resistance in the United Kingdom

Author

Tostevin, A, White, E, Dunn, D, Croxford, S, Delpech, V, Williams, I, Asboe, D, Pozniak, A, Churchill, D, Geretti, AM, Pillay, D, Sabin, C, LeighBrown, A, Smit, E, Aitken, Celia, Cane, Patricia, Chadwick, David, Clark, Duncan, Collins, Simon, Douthwaite, Samuel, Fearnhill, Esther, Porter, Kholoud, Fraser, Christophe, Hale, Antony, Hué, Stéphane, Kaye, Steve, Kellam, Paul, Lazarus, Linda, Mbisa, Tamyo, Mackie, Nicola, Moses, Samuel, Orkin, Chloe, Nastouli, Eleni, Phillips, Andrew, Templeton, Kate, Tilston, Peter, Zhang, Hongyi, Fairbrother, Keith, Greatorex, Jane, OʼShea, Siobhan, Mullen, Jane, Cox, Alison, Tandy, Richard, Fawcett, Tracy, Hopkins, Mark, Ashton, Lynne, Booth, Clare, GarciaDiaz, Ana, Shepherd, Jill, Schmid, Matthias L., Payne, Brendan, Pereira, Spiro, Hubb, Jonathan, Kirk, Stuart, Gunson, Rory, and BradleyStewart, Amanda

Published
2017
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17. Rapid spread and diversification of respiratory syncytial virus genotype ON1, Kenya

Author

Agoti, Charles N., Otieno, James R., Gitahi, Caroline W., Cane, Patricia A., and Nokes, D. James

Subjects
Cladistic analysis -- Health aspects -- Analysis, Infection -- Genetic aspects -- Health aspects -- Analysis, Health
Abstract

Human respiratory syncytial virus (RSV) is the major viral cause of bronchiolitis and pneumonia in infants and also a major cause of severe respiratory illness in the elderly (1). RSV [...]

Published
2014
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21. Low frequency of genotypic resistance in HIV-1-infected patients failing an atazanavir-containing regimen: a clinical cohort study

Author

Dolling, David I., Dunn, David T., Sutherland, Katherine A., Pillay, Deenan, Mbisa, Jean L., Parry, Chris M., Post, Frank A., Sabin, Caroline A., Cane, Patricia A., Aitken, Celia, Asboe, David, Webster, Daniel, Cane, Patricia, Castro, Hannah, Dunn, David, Dolling, David, Chadwick, David, Churchill, Duncan, Clark, Duncan, Collins, Simon, Delpech, Valerie, Geretti, Anna Maria, Goldberg, David, Hale, Antony, Hué, Stéphane, Kaye, Steve, Kellam, Paul, Lazarus, Linda, Leigh-Brown, Andrew, Mackie, Nicola, Orkin, Chloe, Rice, Philip, Pillay, Deenan, Phillips, Andrew, Sabin, Caroline, Smit, Erasmus, Templeton, Kate, Tilston, Peter, Tong, William, Williams, Ian, Zhang, Hongyi, Zuckerman, Mark, Greatorex, Jane, Wildfire, Adrian, OʼShea, Siobhan, Mullen, Jane, Mbisa, Tamyo, Cox, Alison, Tandy, Richard, Hale, Tony, Fawcett, Tracy, Hopkins, Mark, Ashton, Lynn, Booth, Claire, Garcia-Diaz, Ana, Shepherd, Jill, Schmid, Matthias L., Payne, Brendan, Hay, Phillip, Rice, Phillip, Paynter, Mary, Bibby, David, Kirk, Stuart, MacLean, Alasdair, Gunson, Rory, Coughlin, Kate, Fearnhill, Esther, Fradette, Lorraine, Porter, Kholoud, Ainsworth, Jonathan, Anderson, Jane, Babiker, Abdel, Fisher, Martin, Gazzard, Brian, Gilson, Richard, Gompels, Mark, Hill, Teresa, Johnson, Margaret, Kegg, Stephen, Leen, Clifford, Nelson, Mark, Palfreeman, Adrian, Post, Frank, Sachikonye, Memory, Schwenk, Achim, Walsh, John, Huntington, Susie, Jose, Sophie, Thornton, Alicia, Glabay, Adam, Orkin, C., Garrett, N., Lynch, J., Hand, J., de Souza, C., Fisher, M., Perry, N., Tilbury, S., Gazzard, B., Nelson, M., Waxman, M., Asboe, D., Mandalia, S., Delpech, V., Anderson, J., Munshi, S., Korat, H., Welch, J., Poulton, M., MacDonald, C., Gleisner, Z., Campbell, L., Gilson, R., Brima, N., Williams, I., Schwenk, A., Ainsworth, J., Wood, C., Miller, S., Johnson, M., Youle, M., Lampe, F., Smith, C., Grabowska, H., Chaloner, C., Puradiredja, D., Walsh, J., Weber, J., Ramzan, F., Mackie, N., Winston, A., Leen, C., Wilson, A., Allan, S., Palfreeman, A., Moore, A., and Wakeman, K.

Published
2013
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22. A large population sample of African HIV genomes from the 1980s reveals a reduction in subtype D over time associated with propensity for CXCR4 tropism.

Author

Grant, Heather E., Roy, Sunando, Williams, Rachel, Tutill, Helena, Ferns, Bridget, Cane, Patricia A., Carswell, J. Wilson, Ssemwanga, Deogratius, Kaleebu, Pontiano, Breuer, Judith, and Leigh Brown, Andrew J.

Subjects
VIRAL tropism, CXCR4 receptors, HIV, TROPISMS, AFRICANS, GENOMES, AIDS
Abstract

We present 109 near full-length HIV genomes amplified from blood serum samples obtained during early 1986 from across Uganda, which to our knowledge is the earliest and largest population sample from the initial phase of the HIV epidemic in Africa. Consensus sequences were made from paired-end Illumina reads with a target-capture approach to amplify HIV material following poor success with standard approaches. In comparisons with a smaller 'intermediate' genome dataset from 1998 to 1999 and a 'modern' genome dataset from 2007 to 2016, the proportion of subtype D was significantly higher initially, dropping from 67% (73/109), to 57% (26/46) to 17% (82/465) respectively (p < 0.0001). Subtype D has previously been shown to have a faster rate of disease progression than other subtypes in East African population studies, and to have a higher propensity to use the CXCR4 co-receptor ("X4 tropism"); associated with a decrease in time to AIDS. Here we find significant differences in predicted tropism between A1 and D subtypes in all three sample periods considered, which is particularly striking the 1986 sample: 66% (53/80) of subtype D env sequences were predicted to be X4 tropic compared with none of the 24 subtype A1. We also analysed the frequency of subtype in the envelope region of inter-subtype recombinants, and found that subtype A1 is over-represented in env, suggesting recombination and selection have acted to remove subtype D env from circulation. The reduction of subtype D frequency over three decades therefore appears to be a result of selective pressure against X4 tropism and its higher virulence. Lastly, we find a subtype D specific codon deletion at position 24 of the V3 loop, which may explain the higher propensity for subtype D to utilise X4 tropism. [ABSTRACT FROM AUTHOR]

Published
2022
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23. Viral etiology of severe pneumonia among Kenyan infants and children

Author

Berkley, James A., Munywoki, Patrick, Ngama, Mwanajuma, Kazungu, Sidi, Abwao, John, Bett, Anne, Lassauniere, Ria, Kresfelder, Tina, Cane, Patricia A., Venter, Marietjie, Scott, J. Anthony G., and Nokes, D. James

Subjects
Pneumonia in children -- Causes of, Pneumonia in children -- Diagnosis, Pneumonia in children -- Control, Children -- Health aspects, Kenyans -- Health aspects, Respiratory syncytial virus -- Causes of, Diagnostic imaging -- Usage
Abstract

A study was conducted to evaluate and determine the viral etiology of severe pneumonia among Kenyan infants and children using molecular diagnostic techniques. Results indicated that respiratory syncytial virus (RSV) was the predominant viral pathogen in the case of these patients.

Published
2010

25. Long-Term persistence of primary genotypic resistance after HIV-1 serconversion

Author

Pao, David, Dean, Gillian, Green, Tanya, Tang, Alan, Pillay, Deenan, Clarke, Janette, Andrary, Ushan, Fisher, Martin, Drake, Susan, Murphy, Maurice, Kumar, Siva, Underhill, Gillian, White, David, Taylor, Stephen, and Cane, Patricia

Subjects
HIV infection -- Genetic aspects, HIV infection -- Physiological aspects, Drug resistance -- Genetic aspects, Health
Abstract

The drug resistance-associated mutations that persisted over time in the fourteen patients who experienced primary infection with genotypic evidence of resistance, which were followed for up to 3 years is studied. The study concludes that certain resistance-associated mutations are highly stable and these data support the recommendation that all new HIV diagnoses in areas where primary resistance occurs and should undergo genotyping irrespective of whether the date of seroconversion is known.

Published
2004

26. Antigenic and genetic variability of human metapneumoviruses

Author

van den Hoogen, Bernadette G., Herfst, Sander, Sprong, Leo, Cane, Patricia A., Forleo-Neto, Eduardo, de Swart, Rik L., Osterhaus, Albert D.M.E., and Fouchier, Ron A.M.

Subjects
Pneumonia -- Research, Bacterial pneumonia -- Research
Abstract

Human metapneumovirus (HMPV) is a member of the subfamily Pneumovirinae within the family Paramyxoviridae. Other members of this subfamily, respiratory syncytial virus and avian pneumovirus, can be divided into subgroups [...]

Published
2004

32. Detection of drug resistance mutations at low plasma HIV-1 RNA load in a European multicentre cohort study

Author

Prosperi, Mattia C. F., Mackie, Nicola, Di Giambenedetto, Simona, Zazzi, Maurizio, Camacho, Ricardo, Fanti, Iuri, Torti, Carlo, Sönnerborg, Anders, Kaiser, Rolf, Codoñer, Francisco M., Van Laethem, Kristel, Bansi, Loveleen, van de Vijver, David A. M. C., Geretti, Anna Maria, De Luca, Andrea, Giacometti, Andrea, Butini, Luca, del Gobbo, Romana, Menzo, Stefano, Tacconi, Danilo, Corbelli, Giovanni, Zanussi, Stefania, Monno, Laura, Punzi, Grazia, Maggiolo, Franco, Callegaro, Annapaola, Calza, Leonardo, Carla Re, Maria, Pristerà, Raffaele, Turconi, Paola, Mandas, Antonella, Tini, Sauro, Zoncada, Alessia, Paolini, Elisabetta, Amadio, Giorgio, Sighinolfi, Laura, Zuccati, Giuliano, Morfini, Massimo, Manetti, Roberto, Corsi, Paola, Galli, Luisa, Di Pietro, Massimo, Bartalesi, Filippo, Colao, Grazia, Tosti, Andrea, Di Biagio, Antonio, Setti, Maurizio, Bruzzone, Bianca, Penco, Giovanni, Trezzi, Michele, Orani, Anna, Pardelli, Riccardo, De Gennaro, Michele, Chiodera, Alessandro, Scalzini, Alfredo, Palvarini, Loredana, Almi, Paolo, Todaro, Giovanni, dʼArminio Monforte, Antonella, Cicconi, Paola, Rusconi, Stefano, Gismondo, Maria Rita, Gismondo, Maria Rita, Micheli, Valeria, Biondi, Maria Luisa, Gianotti, Nicola, Capetti, Amedeo, Meraviglia, Paola, Boeri, Enzo, Mussini, Cristina, Pecorari, Monica, Soria, Alessandro, Vecchi, Laura, Santirocchi, Maurizio, Brustia, Diego, Ravanini, Paolo, Bello, Federico Dal, Romano, Nino, Mancuso, Salvatrice, Calzetti, Carlo, Maserati, Renato, Filice, Gaetano, Baldanti, Fausto, Francisci, Daniela, Parruti, Giustino, Polilli, Ennio, Sacchini, Daria, Martinelli, Chiara, Consolini, Rita, Vatteroni, Linda, Vivarelli, Angela, Dionisio, Daniele, Nerli, Alessandro, Lenzi, Lucia, Magnani, Giacomo, Ortolani, Patrizia, Andreoni, Massimo, Palamara, Guido, Fimiani, Caterina, Palmisano, Lucia, De Luca, Andrea, Fadda, Giovanni, Vullo, Vincenzo, Turriziani, Ombretta, Montano, Marco, Cenderello, Giovanni, Gonnelli, Angela, Zazzi, Maurizio, Palumbo, Michele, Ghisetti, Valeria, Bonora, Stefano, Foglie, Palma Delle, Rossi, Cristina, Grossi, Paolo, Seminari, Elena, Poletti, Federica, Mondino, Vincenzo, Malena, Marina, Lattuada, Emanuela, Lengauer, Thomas, Däumer, Martin, Hoffmann, Daniel, Kaiser, Rolf, Schülter, Eugen, Müller, Claudia, Oette, Mark, Reuter, Stefan, Esser, Stefan, Fätkenheuer, Gerd, Rockstroh, Jürgen, van de Vijver, David AMC, Incardona, Francesca, Rosen-Zvi, Michal, Lengauer, Thomas, Camacho, Ricardo, Clotet, Bonaventura, Thalme, Anders, Svedhem, Veronica, Bratt, Göran, Gargiulo, Franco, Lapadula, Giuseppe, Manca, Nino, Paraninfo, Giuseppe, Quiros-Roldan, Eugenia, Carosi, Giampiero, Castelnuovo, Filippo, Vandamme, Anne-Mieke, Van Laethem, Kristel, Van Wijngaerden, Eric, Ainsworth, Jonathan, Anderson, Jane, Babiker, Abdel, Dunn, David, Easterbrook, Philippa, Fisher, Martin, Gazzard, Brian, Garrett, Nigel, Gilson, Richard, Gompels, Mark, Hill, Teresa, Johnson, Margaret, Leen, Clifford, Orkin, Chloe, Phillips, Andrew, Pillay, Deenan, Porter, Kholoud, Post, Frank, Sabin, Caroline, Sadiq, Tariq, Schwenk, Achim, Walsh, John, Delpech, Valerie, Palfreeman, Adrian, Dunn, David, Glabay, Adam, Porter, Kholoud, Bansi, Loveleen, Hill, Teresa, Phillips, Andrew, Sabin, Caroline, Orkin, Chloe, Garrett, Nigel, Lynch, Janet, Hand, James, de Souza, Carl, Fisher, Martin, Perry, Nicky, Tilbury, Stuart, Churchill, Duncan, Gazzard, Brian, Nelson, Mark, Waxman, Matthew, Mandalia, Sundhiya, Delpech, Valerie, Anderson, Jane, Kall, Meaghan, Post, Frank, Korat, Hardik, Taylor, Chris, Ibrahim, Fowzia, Campbell, Lucy, Easterbrook, Philippa, Babiker, Abdel, Dunn, David, Glabay, Adam, Porter, Kholoud, Gilson, Richard, James, Laura, Brima, Nataliya, Williams, Ian, Schwenk, Achim, Johnson, Margaret, Youle, Mike, Lampe, Fiona, Smith, Colette, Grabowska, Helen, Chaloner, Clinton, Puradiredja, Dewi Ismajani, Bansi, Loveleen, Hill, Teresa, Phillips, Andrew, Sabin, Caroline, Walsh, John, Weber, Jonathan, Ramzan, Farhan, Carder, Mark, Leen, Clifford, Wilson, Alan, Gompels, Mark, Dooley, Debbie, Palfreeman, Adrian, Anderson, Jane, Asboe, David, Pozniak, Anton, Cameron, Sheila, Cane, Patricia, Chadwick, David, Churchill, Duncan, Clark, Duncan, Collins, Simon, Delpech, Valerie, Pillay, Deenan, Lazarus, Linda, Dunn, David, Dolling, David, Fearnhill, Esther, Castro, Hannah, Porter, Kholoud, Coughlin, Kate, Dolling, David, Zuckerman, Mark, Anna Maria, Geretti, Booth, Clare, Goldberg, David, Gompels, Mark, Hale, Antony, Kaye, Steve, Kellam, Paul, Leigh-Brown, Andrew, Mackie, Nicola, Orkin, Chloe, Pillay, Deenan, Phillips, Andrew, Sabin, Caroline, Smit, Erasmus, Templeton, Kate, Tilston, Peter, Tong, William, Williams, Ian, Zhang, Hongyi, Zhang, Hongyi, Clark, Duncan, Ushiro-Lumb, Ines, Oliver, Tony, Bibby, David, Mitchell, Suzanne, Smit, Erasmus, Mbisa, Tamyo, Wildfire, Adrian, Tandy, Richard, Shepherd, Jill, Chadwick, David, MacLean, Alasdair, Tong, William, Bennett, Diane, Hopkins, Mark, Tilston, Peter, Booth, Clare, Garcia-Diaz, Ana, Kaye, Steve, and Kirk, Stuart

Published
2011
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44. The evolution of HIV-1 reverse transcriptase in route to acquisition of Q151M multi-drug resistance is complex and involves mutations in multiple domains

Author

Gibb Diana M, Parry Chris M, Chintu Chifumbe, Kalumbi Moxmalama, Mulenga Veronica, Kabamba Desire, Gupta Ravi K, Mbisa Jean L, Walker Sarah A, Cane Patricia A, and Pillay Deenan

Subjects
Immunologic diseases. Allergy, RC581-607
Abstract

Abstract Background The Q151M multi-drug resistance (MDR) pathway in HIV-1 reverse transcriptase (RT) confers reduced susceptibility to all nucleoside reverse transcriptase inhibitors (NRTIs) excluding tenofovir (TDF). This pathway emerges after long term failure of therapy, and is increasingly observed in the resource poor world, where antiretroviral therapy is rarely accompanied by intensive virological monitoring. In this study we examined the genotypic, phenotypic and fitness correlates associated with the development of Q151M MDR in the absence of viral load monitoring. Results Single-genome sequencing (SGS) of full-length RT was carried out on sequential samples from an HIV-infected individual enrolled in ART rollout. The emergence of Q151M MDR occurred in the order A62V, V75I, and finally Q151M on the same genome at 4, 17 and 37 months after initiation of therapy, respectively. This was accompanied by a parallel cumulative acquisition of mutations at 20 other codon positions; seven of which were located in the connection subdomain. We established that fourteen of these mutations are also observed in Q151M-containing sequences submitted to the Stanford University HIV database. Phenotypic drug susceptibility testing demonstrated that the Q151M-containing RT had reduced susceptibility to all NRTIs except for TDF. RT domain-swapping of patient and wild-type RTs showed that patient-derived connection subdomains were not associated with reduced NRTI susceptibility. However, the virus expressing patient-derived Q151M RT at 37 months demonstrated ~44% replicative capacity of that at 4 months. This was further reduced to ~22% when the Q151M-containing DNA pol domain was expressed with wild-type C-terminal domain, but was then fully compensated by coexpression of the coevolved connection subdomain. Conclusions We demonstrate a complex interplay between drug susceptibility and replicative fitness in the acquisition Q151M MDR with serious implications for second-line regimen options. The acquisition of the Q151M pathway occurred sequentially over a long period of failing NRTI therapy, and was associated with mutations in multiple RT domains.

Published
2011
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45. Duration of shedding of respiratory syncytial virus in a community study of Kenyan children

Author

Ngama Mwanajuma, White Lisa J, Okiro Emelda A, Cane Patricia A, Medley Graham F, and Nokes D James

Subjects
Infectious and parasitic diseases, RC109-216
Abstract

Abstract Background Our understanding of the transmission dynamics of respiratory syncytial virus (RSV) infection will be better informed with improved data on the patterns of shedding in cases not limited only to hospital admissions. Methods In a household study, children testing RSV positive by direct immunofluorescent antibody test (DFA) were enrolled. Nasal washings were scheduled right away, then every three days until day 14, every 7 days until day 28 and every 2 weeks until a maximum of 16 weeks, or until the first DFA negative RSV specimen. The relationship between host factors, illness severity and viral shedding was investigated using Cox regression methods. Results From 151 families a total of 193 children were enrolled with a median age of 21 months (range 1-164 months), 10% infants and 46% male. The rate of recovery from infection was 0.22/person/day (95% CI 0.19-0.25) equivalent to a mean duration of shedding of 4.5 days (95%CI 4.0-5.3), with a median duration of shedding of 4 days (IQR 2-6, range 1-14). Children with a history of RSV infection had a 40% increased rate of recovery i.e. shorter duration of viral shedding (hazard ratio 1.4, 95% CI 1.01-1.86). The rate of cessation of shedding did not differ significantly between males and females, by severity of infection or by age. Conclusion We provide evidence of a relationship between the duration of shedding and history of infection, which may have a bearing on the relative role of primary versus re-infections in RSV transmission in the community.

Published
2010
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46. Proposal for Human Respiratory Syncytial Virus Nomenclature below the Species Level.

Author

Salimi, Vahid, Viegas, Mariana, Trento, Alfonsina, Agoti, Charles N., Anderson, Larry J., Avadhanula, Vasanthi, Bahl, Justin, Bont, Louis, Brister, J. Rodney, Cane, Patricia A., Galiano, Mónica, Graham, Barney S., Hatcher, Eneida L., Hellferscee, Orienka, Henke, David M., Hirve, Siddhivinayak, Jackson, Sandra, Keyaerts, Els, Kragten-Tabatabaie, Leyla, and Lindstrom, Stephen

Subjects
RESPIRATORY syncytial virus, RESEARCH, BIOLOGICAL evolution, GENETICS, RESEARCH methodology, MEDICAL cooperation, EVALUATION research, COMPARATIVE studies, GENOTYPES, RESPIRATORY syncytial virus infections, MOLECULAR epidemiology
Abstract

Human respiratory syncytial virus (HRSV) is the leading viral cause of serious pediatric respiratory disease, and lifelong reinfections are common. Its 2 major subgroups, A and B, exhibit some antigenic variability, enabling HRSV to circulate annually. Globally, research has increased the number of HRSV genomic sequences available. To ensure accurate molecular epidemiology analyses, we propose a uniform nomenclature for HRSV-positive samples and isolates, and HRSV sequences, namely: HRSV/subgroup identifier/geographic identifier/unique sequence identifier/year of sampling. We also propose a template for submitting associated metadata. Universal nomenclature would help researchers retrieve and analyze sequence data to better understand the evolution of this virus. [ABSTRACT FROM AUTHOR]

Published
2021
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50. An Intensive, Active Surveillance Reveals Continuous Invasion and High Diversity of Rhinovirus in Households.

Author

Kamau, Everlyn, Onyango, Clayton O, Otieno, Grieven P, Kiyuka, Patience K, Agoti, Charles N, Medley, Graham F, Cane, Patricia A, Nokes, D James, and Munywoki, Patrick K

Subjects
RHINOVIRUSES, HOUSEHOLDS
Abstract

We report on infection patterns in 5 households (78 participants) delineating the natural history of human rhinovirus (HRV). Nasopharyngeal collections were obtained every 3–4 days irrespective of symptoms, over a 6-month period, with molecular screening for HRV and typing by sequencing VP4/VP2 junction. Overall, 311/3468 (8.9%) collections were HRV positive: 256 were classified into 3 species: 104 (40.6%) HRV-A; 14 (5.5%) HRV-B, and 138 (53.9%) HRV-C. Twenty-six known HRV types (13 HRV-A, 3 HRV-B, and 10 HRV-C) were identified (A75, C1, and C35 being most frequent). We observed continuous invasion and temporal clustering of HRV types in households (range 5–13 over 6 months). Intrahousehold transmission was independent of clinical status but influenced by age. Most (89.0%) of HRV infection episodes were limited to <14 days. Individual repeat infections were frequent (range 1–7 over 6 months), decreasing with age, and almost invariably heterotypic, indicative of lasting type-specific immunity and low cross-type protection. [ABSTRACT FROM AUTHOR]

Published
2019
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