Abstract
We report that the replication-deficient DY strain of transmissible mink encepalopathy (TME) can delay disease caused by the pathogenic HY TME strain. In this study, competition between the HY and DY TME agents was investigated following superinfection of the sciatic nerve and peritoneal cavity. Initially, DY TME infection was examined in the absence of superinfection and it was found that inoculation into the brain and sciatic nerve resulted in prion disease and PrPSc deposition in brain but not lymphoreticular tissues. Conversely, intraperitoneal inoculation of the DY TME agent did not result in clinical symptoms, DY TME agent replication or PrPSc deposition 400-600 days after infection. These findings indicate that the DY TME agent does not replicate in secondary lymphoid organs and is non-pathogenic when neuroinvasion is dependent on prior infection of the lymphoreticular system. However, intraperitoneal inoculation of the DY TME agent at 60 days, but not at 30 days, prior to intraperitoneal inoculation of the HY TME agent resulted in an extension of the HY TME incubation period. Inoculation of the DY TME agent into the sciatic nerve at 60 days prior to intrasciatic nerve inoculation of the HY TME agent did not delay the incubation period of HY TME. The ability of the DY TME agent to delay HY TME infection following extraneural inoculation, but not neural infection, suggests that HY and DY TME agent competition can occur in a common replication site whose cellular location precedes infection of both the lymphoreticular and peripheral nervous systems.
| Original language | English |
|---|---|
| Pages (from-to) | 265-273 |
| Number of pages | 9 |
| Journal | Journal of General Virology |
| Volume | 85 |
| Issue number | 1 |
| DOIs | |
| State | Published - Jan 2004 |
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All Science Journal Classification (ASJC) codes
- Immunology
- Virology
Cite this
Delay in onset of prion disease for th HY strain of transmissible mink encephalopathy as a result of prior peripheral inoculation with the replication-deficient DY strain. / Bartz, Jason C.; Aiken, Judd M.; Bessen, Richard A.
In: Journal of General Virology, Vol. 85, No. 1, 01.2004, p. 265-273.Research output: Contribution to journal › Article
}
TY - JOUR
T1 - Delay in onset of prion disease for th HY strain of transmissible mink encephalopathy as a result of prior peripheral inoculation with the replication-deficient DY strain
AU - Bartz, Jason C.
AU - Aiken, Judd M.
AU - Bessen, Richard A.
PY - 2004/1
Y1 - 2004/1
N2 - We report that the replication-deficient DY strain of transmissible mink encepalopathy (TME) can delay disease caused by the pathogenic HY TME strain. In this study, competition between the HY and DY TME agents was investigated following superinfection of the sciatic nerve and peritoneal cavity. Initially, DY TME infection was examined in the absence of superinfection and it was found that inoculation into the brain and sciatic nerve resulted in prion disease and PrPSc deposition in brain but not lymphoreticular tissues. Conversely, intraperitoneal inoculation of the DY TME agent did not result in clinical symptoms, DY TME agent replication or PrPSc deposition 400-600 days after infection. These findings indicate that the DY TME agent does not replicate in secondary lymphoid organs and is non-pathogenic when neuroinvasion is dependent on prior infection of the lymphoreticular system. However, intraperitoneal inoculation of the DY TME agent at 60 days, but not at 30 days, prior to intraperitoneal inoculation of the HY TME agent resulted in an extension of the HY TME incubation period. Inoculation of the DY TME agent into the sciatic nerve at 60 days prior to intrasciatic nerve inoculation of the HY TME agent did not delay the incubation period of HY TME. The ability of the DY TME agent to delay HY TME infection following extraneural inoculation, but not neural infection, suggests that HY and DY TME agent competition can occur in a common replication site whose cellular location precedes infection of both the lymphoreticular and peripheral nervous systems.
AB - We report that the replication-deficient DY strain of transmissible mink encepalopathy (TME) can delay disease caused by the pathogenic HY TME strain. In this study, competition between the HY and DY TME agents was investigated following superinfection of the sciatic nerve and peritoneal cavity. Initially, DY TME infection was examined in the absence of superinfection and it was found that inoculation into the brain and sciatic nerve resulted in prion disease and PrPSc deposition in brain but not lymphoreticular tissues. Conversely, intraperitoneal inoculation of the DY TME agent did not result in clinical symptoms, DY TME agent replication or PrPSc deposition 400-600 days after infection. These findings indicate that the DY TME agent does not replicate in secondary lymphoid organs and is non-pathogenic when neuroinvasion is dependent on prior infection of the lymphoreticular system. However, intraperitoneal inoculation of the DY TME agent at 60 days, but not at 30 days, prior to intraperitoneal inoculation of the HY TME agent resulted in an extension of the HY TME incubation period. Inoculation of the DY TME agent into the sciatic nerve at 60 days prior to intrasciatic nerve inoculation of the HY TME agent did not delay the incubation period of HY TME. The ability of the DY TME agent to delay HY TME infection following extraneural inoculation, but not neural infection, suggests that HY and DY TME agent competition can occur in a common replication site whose cellular location precedes infection of both the lymphoreticular and peripheral nervous systems.
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UR - http://www.scopus.com/inward/citedby.url?scp=1642503689&partnerID=8YFLogxK
U2 - 10.1099/vir.0.19394-0
DO - 10.1099/vir.0.19394-0
M3 - Article
VL - 85
SP - 265
EP - 273
JO - Journal of General Virology
JF - Journal of General Virology
SN - 0022-1317
IS - 1
ER -