Epidemiology of the Common Cold in Military Recruits With Emphasis on Infections by Rhinovirus Types 1a, 2, and Two Unclassified Rhinoviruses1

Rosenbaum, Max J.; Berry, P. De; Sullivan, Elizabeth J.; Pierce, Willard E.; Mueller, Rene; Peckenpaugh, R. O.

doi:10.1093/oxfordjournals.aje.a121245

Cited by 26 publications

(25 citation statements)

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“…Some rhinovirus serotypes are isolated much more commonly than others, but this does not necessarily imply that there are true differences in their prevalence, since it may be due merely to the greater ease with which some serotypes can be grown in tissue culture (Roebuck, 1976). Epidemiological studies in 12 4 08 -0 0o L-,J) nursery schoolchildren (Beem, 1969), military recruits (Rosenbaum et al, 1971) and families (Minor et al, 1974b) suggest that infection by one serotype does not generally confer cross-immunity against others.…”

Section: Discussionmentioning

confidence: 99%

Respiratory viral infection and wheezy bronchitis in childhood.

Horn¹,

Brain²,

Gregg³

et al. 1979

Thorax

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The role of respiratory viral infection in wheezy bronchitis was studied in 163 children, aged 0-12 years, in a London general practice. Virological investigations were also performed when these same children had acute upper respiratory illness without wheeze. A virus was isolated in 146 (26.4%/,) of 554 episodes of wheezy bronchitis, rhinoviruses accounting for almost half of the isolations. The relative frequency with which individual viruses were isolated in wheezy bronchitis was similar to that in acute upper respiratory illness in 180 other children who had never had wheezy bronchitis. The large number of isolations of rhinoviruses in wheezy bronchitis is probably due to their numerous serotypes and the absence of cross-immunity between them. Our findings have confirmed that infection by respiratory viruses can provoke wheezy bronchitis in certain children, in whom host factors are an important predeterminant. In children with a previous history of wheezy bronchitis infection by rhinoviruses was associated significantly more often with such an episode than with upper respiratory illness. The maturation of protective mechanisms, including the acquisition of specific immunity to a progressively larger number of viruses, could explain the fall in the age-incidence of wheezy bronchitis.

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Section: Discussionmentioning

confidence: 99%

Respiratory viral infection and wheezy bronchitis in childhood.

Horn¹,

Brain²,

Gregg³

et al. 1979

Thorax

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“…HEV, human enterovirus; EV, echovirus; CV, coxsackievirus; HPV, human poliovirus. (Phillips et al, 1968) URT illness 7,9,13,14,17,56,64 1968 Children (Read et al, 1997) Recurrent asthma 13,29,32,48,49,81 1997 Adult (Military) (Bloom et al, 1963) URT illness 1A, 1B, 2 1963 Adult (Outpatients) (Suzuki et al, 2007) PVOD 40,75,78,80 2007 Adult (Military) (Rosenbaum et al, 1971) Common cold 1A, 2, 38, 7, 64, SD-7407 1971 Adult (Office workers) ARTI 4,9,10,12-14,16,24,35,39 1966 Adult (Lung transplant) (Kaiser et al, 2006) Graft dysfunction 3,27,64 2006 Adult (LTCF) (Louie et al, 2005) LRT illness 82 2005 Adult (Surgery) (Craighead et al, 1969) LRT illness 13 1969 Post-mortem (infants) (Urquhart and Grist, 1972;Urquhart and Stott, 1970SIDS 15, 22 1972 Adult (Isolation) (Holmes et al, 1976) LRT illness 2 1976 Children (isolation) (Stott et al, 1969) LRT illness 1B,10,16,18,19,32,33,38,40,49,51,65,78 1979 URT illness 12,23,50 Children (Krilov et al, 1986) LRT illness 1B,44,53,56,63,88 1986 Children Adults (Reilly et al, 1962) ARTI-Ab NEG for common viruses 10,12,13,18,19,23-25,27,28 1962 7-12,19-22,58 Ab, antibody; ARTI, acute respiratory tract infection; ILI, influenza-like illness; LRT, lower respiratory tract; LTCF, long term care facility; PVOD, post-viral olfactory disease; SD-7407, untyped HRV strain; SIDS, sudden infant death syndrome; URT, upper respiratory tract.…”

Section: Cell Culture Methodsmentioning

confidence: 99%

“…Picornaviruses recognize a variety of receptors (Rossmann, 1994;Khan et al, 2008;Uncapher et al, Minor group HRV strains are underlined, major group are shown in bold. M (only found in HRV A; propensity for monkey cells) and H strains (located in both species; grew in human cell cultures) (Gwaltney and Jordan, 1964;Stott et al, 1969;Rosenbaum et al, 1971;Tyrrell and Parsons, 1960;Tyrrell and Bynoe, 1961;Ketler et al, 1962;Taylor-Robinson and Tyrrell, 1962;Cooney and Kenny, 1977;Bloom et al, 1963) are indicated with superscripts and generally correlate with receptor usage (Macnaughton, 1982). Assignment of some strains to this sub-classification may also have been influenced by the viral load in the inoculum (Douglas et al, 1966a;Hamre, 1967).…”

Section: The Rhinovirionmentioning

confidence: 99%

Human rhinoviruses: The cold wars resume

Mackay

2008

Journal of Clinical Virology

100

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“…This had only rarely been recorded using culture [ 54 ]. HRV RNA has been detected days prior to symptoms commencing and for as long as 5 or more weeks after they cease [ 3 , 258 -261 ].…”

Section: Hrv Shedding and Persistencementioning

confidence: 99%

“…Experimental transmission was also reportedly ineffi cient [ 45 ]. In contrast, "naturally" close-quartered military populations, interacting over 1-4 weeks, experienced rapid spread of HRVs to >50 % of the group [ 54 ]. The use of PCR recently clarifi ed this discrepancy, confi rming that frequent transmission in families is more common than culture-based studies had identifi ed, often resulting in asymptomatic infection among older siblings and parents [ 204 ].…”

Section: Airborne and Intimate Contact Transmissionmentioning

confidence: 99%