Group B coxsackievirus diabetogenic phenotype correlates with replication efficiency.
Group B coxsackieviruses can initiate rapid onset type 1 diabetes (T1D) in old nonobese diabetic (NOD) mice. Inoculating high doses of poorly pathogenic CVB3/GA per mouse initiated rapid onset T1D. Viral protein was detectable in islets shortly after inoculation in association with beta cells as well as other primary islet cell types. The virulent strain CVB3/28 replicated to higher titers more rapidly than CVB3/GA in the pancreas and in established beta cell cultures. Exchange of 5'-nontranslated regions between the two CVB3 strains demonstrated a variable impact on replication in beta cell cultures and suppression of in vivo replication for both strains. While any CVB strain may be able to induce T1D in prediabetic NOD mice, T1D onset is linked both to the viral replication rate and infectious dose.
Kanno
Toru
T
Enterovirus Research Laboratory, Department of Pathology and Microbiology, University of Nebraska Medical Center, 986495 Nebraska Medical Center, Omaha, NE 68198-6495, USA.
Kim
Kisoon
K
Kono
Ken
K
Drescher
Kristen M
KM
Chapman
Nora M
NM
Tracy
Steven
S
D000818:Animals; D003384:Coxsackievirus Infections / Q000150:complications* / Q000473:pathology / Q000821:virology; D003922:Diabetes Mellitus, Type 1 / Q000473:pathology / Q000517:prevention & control*; D029822:Enterovirus B, Human / Q000145:classification / Q000472:pathogenicity / Q000502:physiology*; D007515:Islets of Langerhans / Q000276:immunology / Q000473:pathology / Q000821:virology; D051379:Mice; D016688:Mice, Inbred NOD; D010641:Phenotype; D014779:Virus Replication / Q000502:physiology*