RESUMO
Since 1958 witnessed the detection of Monkeypox virus in monkeys, no human infection was encountered until 1970. Afterwards, zoonotic transmission was the rule near African rainforests, mainly in DRC. Most cases occurred in children who weren't immunized against smallpox. Since 2003 and the first human infection in the USA, research was accelerated. Two clades were identified with different virulence, demographic distribution and transmissibility. The mean age of infection increased with waning smallpox vaccine immunity. Mild febrile prodrome can precede lymphadenopathy, which doesn't occur in smallpox. Homogenous crops of lesions appear in stages until scabs fall and contagiosity ends. However, since May outbreak, cases started to appear in non-endemic areas, human transmission increased and was linked to close sexual contact especially in MSM community. Lesions were found mainly perioral, at genitals and perianal. Newer system for nomenclature was suggested in which there are 3 viral clades and the responsible clade for the outbreak is clade 3 (lineage B.1). About 50 mutations were detected compared with the strains isolated 4 years ago. Gene loss and APOBEC3 may be related to accelerated mutation rate which may accelerate human transmission. Previous mistakes in failure to allocate available vaccines to control the disease in previously endemic areas should be avoided and rapid ring vaccination of potential contacts and those at risk should be a priority. Case isolation, contact isolation or tracing for an incubation period, standard measures for airborne infections and safe sex should be implanted in the light of the current uncertainty.
