TY - CHAP
T1 - Coxsackievirus infections and NOD mice
T2 - Relevant models of protection from, and induction of, type 1 diabetes
AU - Tracy, Steven
AU - Drescher, Kristen M.
PY - 2007/4
Y1 - 2007/4
N2 - Human enteroviruses (HEVs) like the group B coxsackieviruses (CVBs) are prime candidates for infectious, environmental causes of human type 1 diabetes (T1D). Non-obese diabetic (NOD) female mice are well protected from T1D onset if inoculated with CVB when young. Older, prediabetic NOD mice can rapidly develop T1D following inoculation with CVB, mimicking clinical reports of disease-associated T1D onset. The ability to induce rapid T1D in NOD mice is linked to the rate of replication of the CVB strain in β cell cultures and pancreatic tissue, indicating that any CVB strain is potentially diabetogenic under the correct conditions. Rapid T1D onset is preceded by CVB replication in islet cells including β cells. Although CVB strains do not productively infect healthy islets of young mice, CVBs can replicate in healthy islets in the presence of murine IL-4. These models expand much of what is known or suspected regarding the etiologic role of HEVs in human T1D.
AB - Human enteroviruses (HEVs) like the group B coxsackieviruses (CVBs) are prime candidates for infectious, environmental causes of human type 1 diabetes (T1D). Non-obese diabetic (NOD) female mice are well protected from T1D onset if inoculated with CVB when young. Older, prediabetic NOD mice can rapidly develop T1D following inoculation with CVB, mimicking clinical reports of disease-associated T1D onset. The ability to induce rapid T1D in NOD mice is linked to the rate of replication of the CVB strain in β cell cultures and pancreatic tissue, indicating that any CVB strain is potentially diabetogenic under the correct conditions. Rapid T1D onset is preceded by CVB replication in islet cells including β cells. Although CVB strains do not productively infect healthy islets of young mice, CVBs can replicate in healthy islets in the presence of murine IL-4. These models expand much of what is known or suspected regarding the etiologic role of HEVs in human T1D.
UR - http://www.scopus.com/inward/record.url?scp=34249090746&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=34249090746&partnerID=8YFLogxK
U2 - 10.1196/annals.1394.009
DO - 10.1196/annals.1394.009
M3 - Chapter
C2 - 17376828
AN - SCOPUS:34249090746
SN - 1573316784
SN - 9781573316781
T3 - Annals of the New York Academy of Sciences
SP - 143
EP - 151
BT - How Do We Best Employ Animal Models for Type 1 Diabetesand Multiple Sclerosis
PB - Blackwell Publishing Inc.
ER -