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Immunity to homologous rotavirus infection in adult mice: Response
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resolution of rotavirus infection and protection against reinfection in mice. Virology 214, 387–397 Choi, A.H. et al. (1999) Antibodyindependent protection against rotavirus infection of mice stimulated by intranasal immunization with chimeric VP4 or VP6 protein. J. Virol. 73, 7574–7581 Franco, M.A. et al. (1997) Evidence for CD8+ T-cell immunity to murine rotavirus in the absence of perforin, fas and g-interferon. J. Virol. 71, 479–486 McNeal, M.M. et al. (1999) Antibodydependent and -independent protection following intranasal immunization of mice with rotavirus particles. J. Virol. 73, 7565–7573 Franco, M.A. and Greenberg, H.B. (1997) Immunity to rotavirus in T-celldeficient mice. Virology 338, 169–179 McNeal, M.M. et al. (1997) Evidence that resolution of rotavirus infection in mice is due to both CD4 and CD8cell-dependent activities. J. Virol. 71, 8735–8742 Franco, M.A. and Greenberg, H.B. (1995) Role of B cells and cytotoxic T lymphocytes in clearance of and immunity to rotavirus infection in mice. J. Virol. 69, 7800–7806 Franco, M.A. and Greenberg, H.B. (1997) CD8+ T cells can mediate almost complete short term and partial long term immunity to rotavirus in mice. J. Virol. 71, 4165–4180 Chen, S.C. et al. (1998) Protective immunity induced by oral immunization with a rotavirus DNA vaccine encapsulated in microparticles. J. Virol. 72, 5757–5761 Choi, A.H. et al. (1997) Particle bombardment-mediated DNA vaccination with rotavirus VP6 induces high levels of serum rotavirus IgG but fails to protect mice against challenge. Virology 232, 129–138 Feng, N. et al. (1997) Heterotypic protection following oral immunization with live heterologous rotaviruses in a mouse model. J. Infect. Dis. 175, 330–341 Jiang, B. et al. (1999) Heterotypic protection from rotavirus infection in mice vaccinated with virus-like particles. Vaccine 17, 1005–1013 O’Neal, C.M. et al. (1998) Rotavirus 2/6 virus-like particles administered intranasally with cholera toxin, Escherichia coli heat-labile toxin (LT) and LT-R192G induce protection from rotavirus challenge. J. Virol. 72, 3390–3393 Coffin, S.E. et al. (1997) Immunologic correlates of protection against rotavirus challenge after intramuscular immunization of mice. J. Virol. 71, 7851–7856
Immunity to homologous rotavirus infection in adult mice: Response Anthony H-C. Choi, Monica M. McNeal, Matali Basu and Richard L. Ward
F
irstly, we would like to express our appreciation to Franco and Greenberg for highlighting the possibilities and limitations associated with this particular model system. As they point out, since we first developed the model and published our first article on its use1, it has been used by many labs with a variety of mouse and rotavirus stains. Therefore, conclusions drawn with any specific mouse and/or rotavirus set cannot immediately be generalized to other sets. However, if information is not available or cannot be obtained with other sets owing to, for example, a lack of appropriate genetically deficient mouse strains on a particular mouse background, extrapolating the results to the broader picture is a natural course of events. When this is done, the caveats should also be discussed. A case in point is our observation that, following intranasal immunization with either double-layered rotavirus particles2 or VP6 proteins3, together with LT(R192G) as an adjuvant, B-celldeficient mMt mice with a C57BL/6 background are as protected from rotavirus strain EDIM infection as are immunologically normal BALB/c mice. Based on this result, we concluded that protection following intranasal immunization with VP6 in BALB/c mice was unlikely to be antibody dependent. Since that time, this conclusion has been supported by additional evidence (A.H-C. Choi et al., unpublished), namely that both protein fragments and peptides derived from VP6 that do not stimulate detectable serum or stool rotavirus antibodies following intranasal immunization induce nearly complete protection against EDIM shedding in BALB/c mice. To our knowledge, the suggestion by Franco and Greenberg that ‘protective mechanisms identified in C57BL/6 mice probably differ
0966-842X/00/$ - see front matter © 2000 Elsevier Science Ltd. All rights reserved. TRENDS
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from those identified in BALB/c or 129 mice’ can be substantiated only with regard to innate immunity. Clearly, if the same quantity of a specific rotavirus strain is administered to different mouse strains they will shed very different quantities of virus in their stools. For example, in our laboratory, adult C57BL/6 mice administered either culture-adapted or unpassaged EDIM rarely shed detectable amounts of virus. By contrast, both BALB/c and 129 mice shed large quantities of EDIM when challenged as adults. Therefore, their abilities to withstand rotavirus infections as adults clearly differ. The reasons for this could be as simple as differences in available rotavirus receptors on intestinal epithelial cells. There appears to be no compelling evidence that this result regarding innate immunity can be directly extrapolated to conclusions concerning basic differences in mechanisms of learned immunity between mouse strains. However, we acknowledge that this possibility should not be overlooked. A.H-C. Choi, M.M. McNeal, M. Basu and R.L. Ward Divn of Infectious Diseases, CH-1, Children’s Hospital Medical Center, 3333 Burnet Avenue, Cincinnati, OH 45229-3039, USA References 1 Ward, R.L. et al. (1990) Development of an adult mouse model for studies on protection against rotavirus. J. Virol. 64, 5070–5075 2 McNeal, M.M. et al. (1999) Antibodydependent and -independent protection following intranasal immunization of mice with rotavirus particles. J. Virol. 73, 7565–7573 3 Choi, A.H-C. et al. (1999) Antibodyindependent protection against rotavirus infection of mice stimulated by intranasal immunization with chimeric VP4 or VP6 protein. J. Virol. 73, 7574–7581 PII: S0966-842X(99)01683-2 FEBRUARY 2000
4
5
6
7 8
9
10
11
12
13
14
15
16
resolution of rotavirus infection and protection against reinfection in mice. Virology 214, 387–397 Choi, A.H. et al. (1999) Antibodyindependent protection against rotavirus infection of mice stimulated by intranasal immunization with chimeric VP4 or VP6 protein. J. Virol. 73, 7574–7581 Franco, M.A. et al. (1997) Evidence for CD8+ T-cell immunity to murine rotavirus in the absence of perforin, fas and g-interferon. J. Virol. 71, 479–486 McNeal, M.M. et al. (1999) Antibodydependent and -independent protection following intranasal immunization of mice with rotavirus particles. J. Virol. 73, 7565–7573 Franco, M.A. and Greenberg, H.B. (1997) Immunity to rotavirus in T-celldeficient mice. Virology 338, 169–179 McNeal, M.M. et al. (1997) Evidence that resolution of rotavirus infection in mice is due to both CD4 and CD8cell-dependent activities. J. Virol. 71, 8735–8742 Franco, M.A. and Greenberg, H.B. (1995) Role of B cells and cytotoxic T lymphocytes in clearance of and immunity to rotavirus infection in mice. J. Virol. 69, 7800–7806 Franco, M.A. and Greenberg, H.B. (1997) CD8+ T cells can mediate almost complete short term and partial long term immunity to rotavirus in mice. J. Virol. 71, 4165–4180 Chen, S.C. et al. (1998) Protective immunity induced by oral immunization with a rotavirus DNA vaccine encapsulated in microparticles. J. Virol. 72, 5757–5761 Choi, A.H. et al. (1997) Particle bombardment-mediated DNA vaccination with rotavirus VP6 induces high levels of serum rotavirus IgG but fails to protect mice against challenge. Virology 232, 129–138 Feng, N. et al. (1997) Heterotypic protection following oral immunization with live heterologous rotaviruses in a mouse model. J. Infect. Dis. 175, 330–341 Jiang, B. et al. (1999) Heterotypic protection from rotavirus infection in mice vaccinated with virus-like particles. Vaccine 17, 1005–1013 O’Neal, C.M. et al. (1998) Rotavirus 2/6 virus-like particles administered intranasally with cholera toxin, Escherichia coli heat-labile toxin (LT) and LT-R192G induce protection from rotavirus challenge. J. Virol. 72, 3390–3393 Coffin, S.E. et al. (1997) Immunologic correlates of protection against rotavirus challenge after intramuscular immunization of mice. J. Virol. 71, 7851–7856
Immunity to homologous rotavirus infection in adult mice: Response Anthony H-C. Choi, Monica M. McNeal, Matali Basu and Richard L. Ward
F
irstly, we would like to express our appreciation to Franco and Greenberg for highlighting the possibilities and limitations associated with this particular model system. As they point out, since we first developed the model and published our first article on its use1, it has been used by many labs with a variety of mouse and rotavirus stains. Therefore, conclusions drawn with any specific mouse and/or rotavirus set cannot immediately be generalized to other sets. However, if information is not available or cannot be obtained with other sets owing to, for example, a lack of appropriate genetically deficient mouse strains on a particular mouse background, extrapolating the results to the broader picture is a natural course of events. When this is done, the caveats should also be discussed. A case in point is our observation that, following intranasal immunization with either double-layered rotavirus particles2 or VP6 proteins3, together with LT(R192G) as an adjuvant, B-celldeficient mMt mice with a C57BL/6 background are as protected from rotavirus strain EDIM infection as are immunologically normal BALB/c mice. Based on this result, we concluded that protection following intranasal immunization with VP6 in BALB/c mice was unlikely to be antibody dependent. Since that time, this conclusion has been supported by additional evidence (A.H-C. Choi et al., unpublished), namely that both protein fragments and peptides derived from VP6 that do not stimulate detectable serum or stool rotavirus antibodies following intranasal immunization induce nearly complete protection against EDIM shedding in BALB/c mice. To our knowledge, the suggestion by Franco and Greenberg that ‘protective mechanisms identified in C57BL/6 mice probably differ
0966-842X/00/$ - see front matter © 2000 Elsevier Science Ltd. All rights reserved. TRENDS
IN
MICROBIOLOGY
52
VOL. 8
NO. 2
from those identified in BALB/c or 129 mice’ can be substantiated only with regard to innate immunity. Clearly, if the same quantity of a specific rotavirus strain is administered to different mouse strains they will shed very different quantities of virus in their stools. For example, in our laboratory, adult C57BL/6 mice administered either culture-adapted or unpassaged EDIM rarely shed detectable amounts of virus. By contrast, both BALB/c and 129 mice shed large quantities of EDIM when challenged as adults. Therefore, their abilities to withstand rotavirus infections as adults clearly differ. The reasons for this could be as simple as differences in available rotavirus receptors on intestinal epithelial cells. There appears to be no compelling evidence that this result regarding innate immunity can be directly extrapolated to conclusions concerning basic differences in mechanisms of learned immunity between mouse strains. However, we acknowledge that this possibility should not be overlooked. A.H-C. Choi, M.M. McNeal, M. Basu and R.L. Ward Divn of Infectious Diseases, CH-1, Children’s Hospital Medical Center, 3333 Burnet Avenue, Cincinnati, OH 45229-3039, USA References 1 Ward, R.L. et al. (1990) Development of an adult mouse model for studies on protection against rotavirus. J. Virol. 64, 5070–5075 2 McNeal, M.M. et al. (1999) Antibodydependent and -independent protection following intranasal immunization of mice with rotavirus particles. J. Virol. 73, 7565–7573 3 Choi, A.H-C. et al. (1999) Antibodyindependent protection against rotavirus infection of mice stimulated by intranasal immunization with chimeric VP4 or VP6 protein. J. Virol. 73, 7574–7581 PII: S0966-842X(99)01683-2 FEBRUARY 2000