Evolutionary view of the AIDS process.

It is generally accepted that human immunodeficiency virus (HIV) is the etiological agent of acquired immune deficiency syndrome. According to this claim, HIV was transferred to humans from contact with monkeys around 35-50 years ago. However, this claim has not been sufficiently confirmed epidemiologically. The spread and incubation period of the plague epidemic has led to the theory that the Black Death was caused by hemorrhagic viruses. Having examined detailed historical data, we have concluded that the bacterium Yersenia pestis was an infectious agent in the epidemic, together with another agent which we suggest was HIV. Our considerations were mainly based on the existence of the CCR5 delta 32 mutation, which protects against HIV infection and has been present in the Caucasian population for over 2000 years. The combination of two infectious agents led to the devastation of the Black Death, the removal of HIV carriers, and an increase in the number of CCR5Δ32 mutations in the Caucasian population. In sub-Saharan Africa, this epidemic and subsequent sanitation process did not occur, which explains the much higher level of HIV genetic information in this part of the world.

Historical Outbreaks of Simian Hemorrhagic Fever in Captive Macaques Were Caused by Distinct Arteriviruses.

Simian hemorrhagic fever (SHF) is lethal for macaques. Based on clinical presentation and serological diagnosis, all reported SHF outbreaks were thought to be caused by different strains of the same virus, simian hemorrhagic fever virus (SHFV; Arteriviridae). Here we show that the SHF outbreaks in Sukhumi in 1964 and in Alamogordo in 1989 were caused not by SHFV but by two novel divergent arteriviruses. Our results indicate that multiple divergent simian arteriviruses can cause SHF.

Emerging infectious diseases at the beginning of the 21st century.

The emergence and re-emergence of infectious diseases involves many interrelated factors. Global interconnectedness continues to increase with international travel and trade; economic, political, and cultural interactions; and human-to-human and animal-to-human interactions. These interactions include the accidental and deliberate sharing of microbial agents and antimicrobial resistance and allow the emergence of new and unrecognized microbial disease agents. As the 21st century begins, already new agents have been identified, and new outbreaks have occurred. Solutions to limiting the spread of emerging infectious diseases will require cooperative efforts among many disciplines and entities worldwide. This article defines emerging infectious diseases, summarizes historical background, and discusses factors that contribute to emergence. Seven agents that have made a significant appearance, particularly in the 21st century, are reviewed, including: Ebola and Marburg hemorrhagic fevers, human monkeypox, bovine spongiform encephalopathy, severe acute respiratory syndrome (SARS), West Nile virus, and avian influenza. The article provides for each agent a brief historical background, case descriptions, and health care implications.

Emerging infections: lessons from the viral hemorrhagic fevers.

Two Institute of Medicine reports since 1992 have emphasized the dangerous and continuing threat to the world from emerging infectious diseases. Working with viral hemorrhagic fevers provides a number of lessons related to the processes that control emergence, the pattern of disease after emergence, and how to cope with these incidents. This short paper uses two arenavirus hemorrhagic fevers to illustrate some of these principles. Argentine and Bolivian hemorrhagic fevers first came to medical attention in the 1950's. The forces that underlie the emergence of disease in Argentina are not understood, but the Bolivian episode has a reasonably understandable train of events behind it. The Argentine disease had serious impact on the large agricultural economy, and the ecology of the rodent reservoir did not lend itself to control; a vaccine was developed by Argentina and the U.S. with the latter motivated largely by biodefense. The Bolivian disease was controlled in large part by eliminating rodents that invaded towns, and the impact was subsequently below the level needed to trigger drug or vaccine development. These two viruses were important in the recognition of a new family of viruses (Arenaviridae), and this finding of new taxons during the investigation of emerging infectious diseases continues.

History of U.S. military contributions to the study of viral hemorrhagic fevers.

The viral hemorrhagic fever viruses represent a unique group of viruses that can produce large outbreaks of both animal and human disease and produce severe, highly fatal, human illnesses. The viral hemorrhagic fever viruses display a great deal of diversity in their genetic organization, vectors for transmission, and geographic distribution. They share common features in being able to induce a great deal of cellular damage and to elicit an immune response among humans that can result in severe hemorrhage, coagulopathy, shock, and death. The characteristics of the viral hemorrhagic fever viruses as arthropod-borne or rodent-borne viruses that can result in human illnesses with high morbidity and mortality rates make these viruses a unique threat, historically, currently, and in the future, to deployed soldiers around the world. In response to this threat, U.S. military scientists have been world leaders in the development of knowledge on the viral hemorrhagic fever viruses, from extensive fieldwork in areas in which these viruses are endemic, outbreak investigations of epidemics, and careful clinical studies elucidating the pathogenesis of severe disease. Defining the disease threat and creating practical countermeasures through the development of drugs and vaccines has been the major mission of military scientists and has resulted in numerous candidate vaccines currently in animal and human clinical trials.

What caused the Black Death?

For the whole of the 20th century it was believed that the Black Death and all the plagues of Europe (1347-1670) were epidemics of bubonic plague. This review presents evidence that this view is incorrect and that the disease was a viral haemorrhagic fever, characterised by a long incubation period of 32 days, which allowed it to be spread widely even with the limited transport of the Middle Ages. It is suggested that haemorrhagic plague emerged from its animal host in Ethiopia and struck repeatedly at European/Asian civilisations, before appearing as the Black Death. The CCR5-Delta32 mutation confers protection against HIV-1 in an average of 10% of the people of European origin today. It is suggested that all the Deltaccr5 alleles originated from a single mutation event that occurred before 1000 BC and the subsequent epidemics of haemorrhagic plague gently forced up its frequency to 5 x 10(-5) at the time of the Black Death. Epidemics of haemorrhagic plague over the next three centuries then steadily raised the frequency in Europe (but not elsewhere) to present day values.

Reappraisal of the historical selective pressures for the CCR5-Delta32 mutation.

HIV strains are unable to enter macrophages that carry the CCR5-Delta32 deletion; the average frequency of this allele is 10% in European populations. A mathematical model based on the changing demography of Europe from 1000 to 1800 AD demonstrates how plague epidemics, 1347 to 1670, could have provided the selection pressure that raised the frequency of the mutation to the level seen today. It is suggested that the original single mutation appeared over 2500 years ago and that persistent epidemics of a haemorrhagic fever that struck at the early classical civilisations served to force up the frequency to about 5x10(-5) at the time of the Black Death in 1347.

Megadrought and megadeath in 16th century Mexico.

The native population collapse in 16th century Mexico was a demographic catastrophe with one of the highest death rates in history. Recently developed tree-ring evidence has allowed the levels of precipitation to be reconstructed for north central Mexico, adding to the growing body of epidemiologic evidence and indicating that the 1545 and 1576 epidemics of cocoliztli (Nahuatl for "pest") were indigenous hemorrhagic fevers transmitted by rodent hosts and aggravated by extreme drought conditions.

O vírus Ébola e sua infecçäo / The ebola virus and its infection

As propriedades epidemiológicas, ecológicas, biológicas, patogenéticas e o diagnóstico do vírus Ébola e sua infecçåo, bem como seu controle såo apresentadas neste artigo. Embora seja um vírus endêmico em certas regiöes da Africa, o risco de disseminaçåo deste vírus para fora do continente africano tem despertado a atençåo e o interesse da comunidade médica mundial, e acionado a vigilåncia sanitária internacional para este vírus

Clinical and laboratory studies on haemorrhagic fever in Burma, 1970-72.

This three-year serologic study of 2 060 children with a clinical diagnosis of haemorrhagic fever, who were admitted to the Children's Hospital and other hospitals in Rangoon, has shown that the etiology of the illness was multiple. Of all these patients, 347 (16.8%) had a dengue infection (96 with primary and 251 with secondary dengue infections), 510 (24.7%) had chikungunya infections, 55 (2.7%) had simultaneous chikungunya and dengue, 263 (12.8%) had influenza A infections, 62 (3.0%) had influenza B, 12 (0.6%) had measles, and there were 811 (39.4%) for whom no etiology could be established. Epidemiological and clinical features and laboratory findings are discussed. Evidence is presented for human infections with all four types of denguevirus in Rangoon.