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Identifying the Conditions Under Which Antibodies Protect Against Infection by Equine Infectious Anemia Virus.

Schwartz EJ, Smith RJ - Vaccines (Basel) (2014)

Bottom Line: A more complete understanding is needed of antibody protection against lentivirus infection, as well as the role of mutation in resistance to an antibody vaccine.In addition, a three-strain competition model is considered in which a second mutant strain may coexist with the first mutant strain.The conditions that permit viral escape by the mutant strains are determined, as are the effects of variation in the model parameters.

View Article: PubMed Central - PubMed

Affiliation: School of Biological Sciences and Department of Mathematics, Washington State University, Pullman, WA 99164, USA. ejs@wsu.edu.

ABSTRACT
The ability to predict the conditions under which antibodies protect against viral infection would transform our approach to vaccine development. A more complete understanding is needed of antibody protection against lentivirus infection, as well as the role of mutation in resistance to an antibody vaccine. Recently, an example of antibody-mediated vaccine protection has been shown via passive transfer of neutralizing antibodies before equine infectious anemia virus (EIAV) infection of horses with severe combined immunodeficiency (SCID). Viral dynamic modeling of antibody protection from EIAV infection in SCID horses may lead to insights into the mechanisms of control of infection by antibody vaccination. In this work, such a model is constructed in conjunction with data from EIAV infection of SCID horses to gain insights into multiple strain competition in the presence of antibody control. Conditions are determined under which wild-type infection is eradicated with the antibody vaccine. In addition, a three-strain competition model is considered in which a second mutant strain may coexist with the first mutant strain. The conditions that permit viral escape by the mutant strains are determined, as are the effects of variation in the model parameters. This work extends the current understanding of competition and antibody control in lentiviral infection, which may provide insights into the development of vaccines that stimulate the immune system to control infection effectively.

No MeSH data available.


Related in: MedlinePlus

The case when the mutation rate of Mutant 2 is high (ϵ2 = 2.7 × 101). Here, Mutant 1 has 10-fold resistance to the antibodies, Mutant 2 has 100-fold resistance to the antibodies and m = 10, recreating the conditions of Figure 3B, Figure 4B and Figure 5B (i.e., the cases of 10-fold magnification), except for the high mutation rate of Mutant 2. (A) Unlike Figure 3B, Mutant 2 escapes; (B) unlike Figure 4B, Mutant 1 persists; conversely, Mutant 2 is eradicated, despite its extremely high mutation rate; (C) the persistence of Mutant 1, similar to Figure 5B.
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vaccines-02-00397-f006: The case when the mutation rate of Mutant 2 is high (ϵ2 = 2.7 × 101). Here, Mutant 1 has 10-fold resistance to the antibodies, Mutant 2 has 100-fold resistance to the antibodies and m = 10, recreating the conditions of Figure 3B, Figure 4B and Figure 5B (i.e., the cases of 10-fold magnification), except for the high mutation rate of Mutant 2. (A) Unlike Figure 3B, Mutant 2 escapes; (B) unlike Figure 4B, Mutant 1 persists; conversely, Mutant 2 is eradicated, despite its extremely high mutation rate; (C) the persistence of Mutant 1, similar to Figure 5B.

Mentions: We also examined the case when the mutation rate of Mutant 2 (ϵ2) was significantly higher than the mutation rate of Mutant 1 (ϵ1) for the case when Mutant 1 had 10-fold resistance and Mutant 2 had 100-fold resistance. Figure 6 is the analogue of Figure 3B, Figure 4B and Figure 5B (i.e., when m = 10), but with a high mutation rate of Mutant 2. Figure 6A shows that Mutant 2 can escape if its mutation rate is sufficiently high, which is not surprising. Figure 6C is qualitatively unchanged from Figure 5B.


Identifying the Conditions Under Which Antibodies Protect Against Infection by Equine Infectious Anemia Virus.

Schwartz EJ, Smith RJ - Vaccines (Basel) (2014)

The case when the mutation rate of Mutant 2 is high (ϵ2 = 2.7 × 101). Here, Mutant 1 has 10-fold resistance to the antibodies, Mutant 2 has 100-fold resistance to the antibodies and m = 10, recreating the conditions of Figure 3B, Figure 4B and Figure 5B (i.e., the cases of 10-fold magnification), except for the high mutation rate of Mutant 2. (A) Unlike Figure 3B, Mutant 2 escapes; (B) unlike Figure 4B, Mutant 1 persists; conversely, Mutant 2 is eradicated, despite its extremely high mutation rate; (C) the persistence of Mutant 1, similar to Figure 5B.
© Copyright Policy
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC4494265&req=5

vaccines-02-00397-f006: The case when the mutation rate of Mutant 2 is high (ϵ2 = 2.7 × 101). Here, Mutant 1 has 10-fold resistance to the antibodies, Mutant 2 has 100-fold resistance to the antibodies and m = 10, recreating the conditions of Figure 3B, Figure 4B and Figure 5B (i.e., the cases of 10-fold magnification), except for the high mutation rate of Mutant 2. (A) Unlike Figure 3B, Mutant 2 escapes; (B) unlike Figure 4B, Mutant 1 persists; conversely, Mutant 2 is eradicated, despite its extremely high mutation rate; (C) the persistence of Mutant 1, similar to Figure 5B.
Mentions: We also examined the case when the mutation rate of Mutant 2 (ϵ2) was significantly higher than the mutation rate of Mutant 1 (ϵ1) for the case when Mutant 1 had 10-fold resistance and Mutant 2 had 100-fold resistance. Figure 6 is the analogue of Figure 3B, Figure 4B and Figure 5B (i.e., when m = 10), but with a high mutation rate of Mutant 2. Figure 6A shows that Mutant 2 can escape if its mutation rate is sufficiently high, which is not surprising. Figure 6C is qualitatively unchanged from Figure 5B.

Bottom Line: A more complete understanding is needed of antibody protection against lentivirus infection, as well as the role of mutation in resistance to an antibody vaccine.In addition, a three-strain competition model is considered in which a second mutant strain may coexist with the first mutant strain.The conditions that permit viral escape by the mutant strains are determined, as are the effects of variation in the model parameters.

View Article: PubMed Central - PubMed

Affiliation: School of Biological Sciences and Department of Mathematics, Washington State University, Pullman, WA 99164, USA. ejs@wsu.edu.

ABSTRACT
The ability to predict the conditions under which antibodies protect against viral infection would transform our approach to vaccine development. A more complete understanding is needed of antibody protection against lentivirus infection, as well as the role of mutation in resistance to an antibody vaccine. Recently, an example of antibody-mediated vaccine protection has been shown via passive transfer of neutralizing antibodies before equine infectious anemia virus (EIAV) infection of horses with severe combined immunodeficiency (SCID). Viral dynamic modeling of antibody protection from EIAV infection in SCID horses may lead to insights into the mechanisms of control of infection by antibody vaccination. In this work, such a model is constructed in conjunction with data from EIAV infection of SCID horses to gain insights into multiple strain competition in the presence of antibody control. Conditions are determined under which wild-type infection is eradicated with the antibody vaccine. In addition, a three-strain competition model is considered in which a second mutant strain may coexist with the first mutant strain. The conditions that permit viral escape by the mutant strains are determined, as are the effects of variation in the model parameters. This work extends the current understanding of competition and antibody control in lentiviral infection, which may provide insights into the development of vaccines that stimulate the immune system to control infection effectively.

No MeSH data available.


Related in: MedlinePlus