Abstract
The use of recombinant viral vectors expressing T. gondii antigens is a safe and efficient approach to induce immune response against the parasite and a valuable tool for vaccine development. We have previously protected mice from toxoplasmosis by immunizing the animals with an adenovirus expressing the protein SAG1 (AdSAG1) of T. gondii. We are now looking for ways to improve the vaccination strategy and enhance protection. One limitation of homologous vaccinations (sequential doses of the same vector) is induction of anti-vector immune response that blocks cell transduction, restricts transgene expression and, consequently, compromises the overall outcome of vaccination. One way to avert the effects of anti-vector response is to use different viruses in prime and boost (heterologous vaccination). Bearing this in mind, we generated a modified Vaccinia Virus Ankara encoding SAG1 (MVASAG1), to be tested as boost agent after prime with AdSAG1. Although minor differences were observed in the magnitude of the anti-SAG1 immune response induced by each vaccination protocol, the heterologous immunization with AdSAG1 followed by MVASAG1 resulted in improved capacity to control brain cyst formation in a model of chronic toxoplasmosis in C57BL/6 mice.
Highlights
Toxoplasma gondii is an obligate intracellular protozoan that belongs to Phylum Apicomplexa
The recombinant modified Vaccinia Virus Ankara encoding SAG1 (MVASAG1) was generated by homologous intracellular recombination between the plasmid pLW44 encoding the Sag1 gene and the genome from a wild type modified Vaccinia virus Ankara (MVA)
The success of a recombinant vaccine depends on many factors, including identification and selection of those parasite components targeted by host immune system and the design of powerful vectors that can induce efficient ‘‘in vivo’’ expression of those antigens
Summary
Toxoplasma gondii is an obligate intracellular protozoan that belongs to Phylum Apicomplexa. Infection of all types of hosts may occur through consumption of meat and viscera of animals infected with T. gondii, or through ingestion of water/vegetables contaminated by sporulated oocysts [2]. In both intermediate and definitive hosts, infection is followed by a short period of intense replication of tachyzoites, which culminates with rupture of infected cells and parasite spreading from the initial infection site. The tachyzoites later convert into slow-replicating bradyzoites that become enclosed in intracellular cysts This stage conversion characterizes the chronic form of toxoplasmosis, which can persist through the entire life of the host [3]. There are studies suggesting an important role for antibodies during acute phase of infection [6], and others pointing for a minor influence of immunoglobulins in parasite control during chronic disease [7]
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