Why Did They Not Die?

Letter to Editor

Austin J Public Health Epidemiol. 2021; 8(3): 1106.

Why Did They Not Die?

Ishak R¹*, Guerreiro JF² and Vallinoto ACR¹

1Virus Laboratory, Institute of Biological Sciences, Federal University of Pará, Belém, Guamá, Pará, Brazil

2Laboratory of Human and Medical Genetics, Institute of Biological Sciences, Federal University of Pará, Belém, Guamá, Pará, Brazil

*Corresponding author: Ricardo Ishak, Virus Laboratory, Institute of Biological Sciences, Federal University of Pará; Belém, 66.075-110, Guamá, Pará, Brazil

Received: August 08, 2021; Accepted: August 17, 2021; Published: August 24, 2021

Letter to Editor

By 1992, Francis Black published an article that investigated the question in the tittle (Why did they die?). The article suggested that the low genetic diversity of the indigenous populations helped to explain why infectious diseases threatened the survival of vulnerable indigenous groups distributed in the Amazon region of Brazil [1]. At that time, only traditional methodological tools were available to explain the influence of the genetic similarities within families residing in isolated indigenous communities. The emerging knowledge of the Human Leukocyte Antigen (HLA), Class I Major Histocompatibility Complex (MHC) A and B loci genes could explain the higher risk of infectious agents in indigenous populations compared to that of urban population groups [1].

Colonization brought violence, slavery and diseases to natives inhabiting the Brazilian territory. Indigenous population numbers were drastically reduced, although surviving groups did maintain enough population growth to keep these populations demographically viable [2,3]. The contact with novel infectious agents, particularly with measles and influenza, led to a high mortality and devastating social changes in the community [1].

Isolated population groups do not generally have endemic viruses, but epidemics can occur with the occasional introduction that can infect many susceptible persons [4]. The entry of new infectious agents may be due to the demographic modifications of small groups. The lack of genetic diversity within these populations is a common explanation for the occurrence of epidemics with high mortality rates [4]. In contrast, only a few genetic traits and genes have been shown to be involved in the mechanisms of susceptibility among indigenous population groups. The decrease in the number of epidemics among indigenous peoples in the recent past is also important to consider, and this was caused by an improvement in the access to health care [3].

The recent emergence and rapidly spread of the RNA virus, severe acute respiratory syndrome coronavirus 2 or SARS-CoV-2, which infects the respiratory tract, reinstated the concern for these vulnerable population groups, particularly the indigenous peoples from the Amazon region of Brazil. The history of past epidemics caused the health authorities to rapidly take action [5,6].

Seroepidemiological investigations are underway among urban groups in Brazil, but few of these investigations are being pursued in indigenous peoples. Recent results [7] have showed an extensive presence of antibodies against SARS-CoV-2 in the population of Xikrin do Bacajá (prevalence of 74.5%). The continuing surveillance of populations have determined that the prevalence of antibodies among six indigenous groups in the state of Pará (Asurini do Koatinemo, Araweté, Parakanã, Munduruku and Kararaô) ranges from the absence of antibodies to close to 80% (A C R Vallinoto ongoing investigation). One single death associated with COVID-19 (coronavirus disease 2019) was reported in an elderly chief of the village in Xikrin do Bacajá; among the other 742 infections undergoing investigations, there were five deaths in Munduruku and one in Parakanã.

Similar to the general question from Black’s original article, these facts now pose a main question against all the odds: why did they not die?

Updated data on the COVID-19 pandemic in indigenous peoples in Brazil, reported in the Epidemiological Bulletin of the Special Secretariat for Indigenous Health – SESAI (http://www. saudeindigena.net.br/coronavirus/mapaEp.php), show that to date 51,709 cases of SARS-CoV-2 infection have been confirmed in the 34 Special Indigenous Health Districts (DSEI), with only 762 deaths (mortality rate of 1.47%); below the national average for urban populations (2.8% - https://covid.saude.gov.br).

It is possible that a low heterogeneity among the indigenous peoples, as compared to the trihybrid Amazonian populations [8], is associated with a poor response to infectious agents and diseases. Until the 1990s, our associates at the genetic laboratory were using protein polymorphisms, and it was quite evident that there were different manifestations of Hepatitis B virus (HBV) and Chlamydia exposure, infection and agent/host interactions resulting in persistence among the different indigenous groups [9,10]. The urban communities showed a different response when communities were tested for both agents.

A high exposure to both agents also results in high levels of persistence of the infectious agents. However, it also showed that a low exposure to the agents caused higher levels of persistence and vice versa, as shown in Table 1. For instance, Tiryió had a low prevalence of exposure to HBV and Chlamydia, but these areas maintained medium and high levels of persistence of HBV and Chlamydia, respectively. The nature of the agents (virus vs. bacterium) have different genetic complexities, and different infectious agents can be more or less virulent, possibly by avoiding the immunological responses in individuals. These agents can cause different degrees of outcome severity, which can be different from what was expected.

Citation: Ishak R, Guerreiro JF and Vallinoto ACR. Why Did They Not Die?. Austin J Public Health Epidemiol. 2021; 8(3): 1106.