KSHV infects only humans, but no other species, including mice [22], [23], [24] and [25]. One study demonstrated that repeated intravenous immunizations of KSHV to NOD/SCID mice resulted in the establishment of latent KSHV infection; LANA-1 was immunohistochemically detected in the spleen of the mice in that report [24]. A recent study showed KSHV infected common marmosets [9]. However, there is currently no report describing successful KSHV infection in immunocompetent small

animals. Thus, development of a new animal model is an important issue to estimate the efficacy of KSHV vaccine. The seroprevalence of KSHV among the general population is extremely low compared with other herpes viruses [4] and [20]. Seropositivity of KSHV among the Japanese general population is about 1%, whereas many adults have antibodies to herpes simplex virus-1 (55–63%), varicella zoster virus (almost 100%), Epstein-Barr Smad inhibitor virus (>90%), cytomegalovirus Olaparib chemical structure (95% in pregnant women), and HHV-6 (79%) in Japan [4], [39], [40], [41], [42] and [43]. Since vaccine is generally effective for prevention of de novo infection of virus, a vaccine strategy could be effective for the prevention of KSHV infection in KSHV-uninfected individuals. Epidemiological data revealed that KSHV is widespread among MSM [3]. However, 40% of HIV-infected MSM were KSHV-uninfected

in Japan [4]. In addition, vaccine should have some effect on the prevention of virus reactivation. In that sense, KSHV vaccine may have some effects on KSHV-infected individuals to prevent occurrence of KS. Thus, KSHV vaccine should be a promising tool for prophylaxis of KS. The present study provides a part of the fundamental data of animal experiments on KSHV. Further studies are required to develop the KSHV vaccine. The authors

thank Dr. Jeffrey Vieira, Department of Laboratory Medicine, University of Washington, for providing the recombinant KSHV. This study was supported by a grant for Research on Publicly Essential Drugs and Medical Devices from the Japan Health Sciences Foundation (No. SAA4832). “
“Zoonotic visceral leishmaniasis (VL), caused by the protozoan parasite Leishmania infantum (chagasi), is a vector-borne disease found in South Rolziracetam America and areas surrounding the Mediterranean Sea [1] and [2]. Dogs are the major reservoirs for L. infantum in these regions [3] and [4], and control of the disease in dogs could have a significant impact on human disease [5], [6], [7] and [8]. Beginning in the 1960s, Brazilian health authorities began culling infected dogs in the largest endemic areas of northeast Brazil as a major strategy for reducing transmission to humans [9]. However, judging from the prevalence of VL in humans and its recent spread into several metropolitan areas [10] and [11], this strategy has been inadequate.