TY - JOUR
T1 - Dynamics of HIV infection in lymphoid tissue network
AU - Nakaoka, Shinji
AU - Iwami, Shingo
AU - Sato, Kei
N1 - Funding Information:
The authors are grateful to the referees for constructive and helpful comments and suggestions, which led to significant improvement of our original manuscript. This research was partly supported by (i) the Japan Society for the Promotion of Science (JSPS) through the "Grant-in-Aid for Young Scientists B25871132 (to S.N.) and B25800092 (to S.I.)", and received funding support from the Commissioned Research program of the Ministry of Health, Labour and Welfare, Japan (to S.N., H26-ShinkoJitsuyoka-General-016).
Publisher Copyright:
© 2015, Springer-Verlag Berlin Heidelberg.
PY - 2016/3/1
Y1 - 2016/3/1
N2 - Human immunodeficiency virus (HIV) is a fast replicating ribonucleic acid virus, which can easily mutate in order to escape the effects of drug administration. Hence, understanding the basic mechanisms underlying HIV persistence in the body is essential in the development of new therapies that could eradicate HIV infection. Lymphoid tissues are the primary sites of HIV infection. Despite the recent progress in real-time monitoring technology, HIV infection dynamics in a whole body is unknown. Mathematical modeling and simulations provide speculations on global behavior of HIV infection in the lymphatic system. We propose a new mathematical model that describes the spread of HIV infection throughout the lymphoid tissue network. In order to represent the volume difference between lymphoid tissues, we propose the proportionality of several kinetic parameters to the lymphoid tissues’ volume distribution. Under this assumption, we perform extensive numerical computations in order to simulate the spread of HIV infection in the lymphoid tissue network. Numerical computations simulate single drug treatments of an HIV infection. One of the important biological speculations derived from this study is a drug saturation effect generated by lymphoid network connection. This implies that a portion of reservoir lymphoid tissues to which drug is not sufficiently delivered would inhibit HIV eradication despite of extensive drug injection.
AB - Human immunodeficiency virus (HIV) is a fast replicating ribonucleic acid virus, which can easily mutate in order to escape the effects of drug administration. Hence, understanding the basic mechanisms underlying HIV persistence in the body is essential in the development of new therapies that could eradicate HIV infection. Lymphoid tissues are the primary sites of HIV infection. Despite the recent progress in real-time monitoring technology, HIV infection dynamics in a whole body is unknown. Mathematical modeling and simulations provide speculations on global behavior of HIV infection in the lymphatic system. We propose a new mathematical model that describes the spread of HIV infection throughout the lymphoid tissue network. In order to represent the volume difference between lymphoid tissues, we propose the proportionality of several kinetic parameters to the lymphoid tissues’ volume distribution. Under this assumption, we perform extensive numerical computations in order to simulate the spread of HIV infection in the lymphoid tissue network. Numerical computations simulate single drug treatments of an HIV infection. One of the important biological speculations derived from this study is a drug saturation effect generated by lymphoid network connection. This implies that a portion of reservoir lymphoid tissues to which drug is not sufficiently delivered would inhibit HIV eradication despite of extensive drug injection.
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U2 - 10.1007/s00285-015-0940-x
DO - 10.1007/s00285-015-0940-x
M3 - Article
C2 - 26507442
AN - SCOPUS:84958104308
SN - 0303-6812
VL - 72
SP - 909
EP - 938
JO - Journal of Mathematical Biology
JF - Journal of Mathematical Biology
IS - 4
ER -