Division of Infectious Diseases

Joseph M. Vinetz, M.D.

Joseph M. Vinetz, M.D.
Professor of Medicine, University of California, San Diego (UCSD)

9500 Gilman Drive
Mail Code 0741

Palade Laboratories, Room 125
La Jolla, CA 92092-0741

Telephone: (858) 822-5320
Fax: (858) 822-5322
Email: jvinetz@ucsd.edu

Molecular Pathology Website

Background

Dr. Vinetz received his B.S. from Yale University, his M.D. from the UCSD School of Medicine, and did his residency in Internal Medicine at the Johns Hopkins School of Medicine. He did his Infectious Diseases Fellowship training at Johns Hopkins with the research component carried out in the Malaria Vaccines Section of the Laboratory of Parasitic Disease at the National Institutes of Health. After being on the faculty of the WHO Center for Tropical Diseases at the University of Texas Medical Branch in Galveston, he joined the faculty at UCSD School of Medicine as Associate Professor in 2003.

Research Interests

We currently study two tropical infectious diseases, malaria and leptospirosis, both at UCSD and through internationally-based collaborations. My laboratory has both basic science and translational research components, taking a comprehensive, integrated to our research.

Malaria:

Malaria is among the three most important causes of global morbidity and mortality, affecting hundreds of millions of people in Africa, Asia, and South America yearly, and leading to millions of deaths annually. Drug resistance to standard anti-malarial drugs is increasing and no deployable malaria vaccine has been produced. There is major emphasis in governmental and private funding agencies on malaria research to address this major ongoing public health threat.

With a newly funded 5 year grant from the NIH, "Human Reservoirs of Plasmodium vivax Transmission in the Peruvian Amazon," our field-based malaria research focuses on developing an integrated strategy to interrupt malaria transmission. This project is a collaborative effort of UCSD, Universidad Peruana Cayetano Heredia in Lima, Peru, Johns Hopkins School of Public Health, Asociacion Benefica PRISMA, and the U.S. Naval Medical Research Center Detachment, Lima, Peru. The long-term goal of this project is to determine specific epidemiological characteristics of P. vivax transmission and human reservoirs of maintaining P. vivax transmission in the Peruvian Amazon region towards the rational deployment of a transmission-blocking vaccine. This project will test the hypothesis that introduction of exogenous P. vivax into local populations is responsible for continuing transmission in rural villages surrounding Iquitos, Peru, the capital of the Peruvian Amazon. Alternative hypotheses are 1) that relapsing P. vivax malaria is the source for maintaining local transmission; or 2) there is simply continuous transmission of already locally established genotypes within local populations. Specific aim 1 is to determine circulating Plasmodium vivax genotypes at the individual village level through prospective, population-based surveillance of people with P. vivax parasitemia. Changes or stability of P. vivax genotypes will be assessed over space and time using recently validated genetic markers. Specific aim 2 is to determine transmission dynamics of P. vivax using geographic spatio- temporal analysis of circulating genotypes using spatial statistical modeling and cluster analysis. These analyses will distinguish whether circulating P. vivax genotypes are already established in villages (either continuously circulating or resulting from relapsing P. vivax from hypnozoites) or are newly introduced by infected inhabitants returning from travel away from the village. Specific aim 3 is to determine whether transmission-blocking immunity develops in the Peruvian Amazon population to potentially modify P. vivax transmission dynamics. Membrane feeding studies will be performed using local Anopheles darlingi mosquitoes and local P. vivax patients as sources of parasites, and by experimental infections of Anopheles mosquitoes from splenectomized non-human primates infected experimentally with P. vivax. In vitro assays (ELISA, IFA) will be used to determine the validity of the in vivo mosquito infection assay. These data will provide the basis for planning transmission-blocking interventions and elimination of human reservoirs of P. vivax, and provide a rational basis for determining strategies to implement and deploy new transmission- blocking vaccines as one approach towards the future elimination of P. vivax malaria from the Amazon basin.

With a newly renewed 5 year NIH grant, our basic malaria research focuses on molecular, cellular and biochemical mechanisms by which the malaria parasite (the ookinete) stage invades the mosquito midgut; the long-term goal is to develop strategies of blocking malaria transmission from humans to mosquitoes. The genome of the lethal human malaria parasite, Plasmodium falciparum has been sequenced, as well as that of the major mosquito vector, Anopheles gambiae . In addition, other Plasmodium genomes of parasites used to study animal models of malaria have been sequenced, including our collaboration with the Sanger Centre in Cambridge, U.K. to sequence the genome of the avian malaria parasite, Plasmodium gallinaceum, which is a major model for detailed mechanistic studies of malaria transmission to mosquitoes. We also have ongoing proteomics projects in collaboration with John Yates, Ph.D. and colleagues of the Scripps Research Institute to define the ookinete proteome. These projects in genomics and proteomics are at the cutting edge of the field, and are timely resources and an amazing scientific environment for highly motivated trainees interested in exploring the cutting edge of a field of global importance.

Leptospirosis:

Leptospirosis is a zoonotic disease caused by spirochetes of the genus Leptospira, which are transmitted from infected mammals (wild and domestic) to humans via infected urine. Our studies range from epidemiology and ecology to immunology to molecular pathogenesis. One of the major questions we are addressing is why some patients with leptospirosis develop only inapparent infection or mild febrile disease, while others develop fulminant jaundice, renal failure, hemorrhage, meningitis and.or myocarditis/heart failure.

With two newly funded grants from the NIH, we are actively investigating molecular and genetic changes aspects of Leptospira and the human host response in leptospirosis predisposing to severe disease. In our field site in the Peruvian Amazon region of Iquitos, we have found leptospirosis to cause far more infection and morbidity than the other presumed causes of febrile illness such as malaria or dengue. In Sao Paulo, Brazil, where severe leptospirosis is a major public health threat, we are investigating possible genetic reasons that most leptospirosis patients do not develop severe disease, while a small minority do.

Selected Publications

Click here to view Dr. Vinetz' CV.