VZV Population Dynamics.

Varicella Zoster Virus (VZV) is an ubiquitous virus from the herpesviruses family. Susceptible individuals that are infected express a clinical manifestation known as varicella (or chickenpox). The virus then establishes latency and remains like this for many years.The mechanism(s) that trigger reactivation is not well known, but in the elderly it has been observed that when cell-mediated immunity wanes, the virus is reactivated and cause herpes zoster (also known as shingles). It has been assumed for many years that the infectivity of an individual with herpes zoster is very low relatively to a individual with varicella. So, the 1rst mathematical model developed in 1995 to measured the impact of the introduction of a vaccine in the USA on the dynamics of the VZV did not account for the infectiousness of zoster. Later, others proved that without this infectiouness due to zoster we could not explain the persistence of the virus in small populations.The interest in studying the dynamics of VZV has been raised because there is a pressure to introduce mass vaccination strategies into several countries to reduce the number of varicella cases and zoster, responsible for a large number of hospital admissions. Nonetheless recent mathematical models that incorporate more precise information about the latency period predict that there could be a raise in the number of zoster cases due to vaccination reducing the vaccine cost-efectiveness. In this seminar I intend to review the dynamics of the models already developed and explain the results by considering a reinfection threshold.

Why is progression into AIDS so slow?

In HIV research there are two intriguing, yet poorly understood, observations. The first is the very slow pace of progression into AIDS, which can take more than a decade. The second is that HIV-1 and HIV-2 infected individuals with identical immunological parameters will progress into AIDS at very different rates. With the purpose of explaining these two observations, it was developed several mathematical models describing different pathogenesis mechanisms discussed in the literature, and confronted them with experimental data. The results indicate that the slow pace of HIV infection might reflect the clonal heterogeneity of the CD4 pool, irrespectively of whether CD4 depletion is caused by virus-associated cytopathicity or by chronic activation. Under this scenario, the different progression rates of HIV-1 and HIV-2 infections could be simply explained by a differential transmission rate of the two viruses within the CD4 pool.

1. Pattern formation in Epidemiological models<\p>

2. Modeling TB - resistant vs. sensitive

1. Pattern formation in Epidemiological models

I am considering spatially extended models for diseases with temporary immunity or partial immunity. Results so far indicate that spatial patterning occurs more generally under temporary immunity than under partial immunity.

2. Modeling TB - resistant vs. sensitive

Recent data confirms that the incidence of tuberculosis has been rising throughout the world and this has been accompanied by an increase in drug resistance. I plan to build possible scenarios for strains interactions and investigate the associated epidemiological behaviors.

Reevaluation of the Recycling Hypothesis in the Germinal Center Reactions.

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