INTRODUCTION
Dengue fever (DF) is a tropical disease caused by the dengue virus (DENV) belonging to the Flaviviridae family 1. Considered a zoonotic arbovirus, it is mainly transmitted by the female mosquitoes of the Aedes aegypti species, and to a lesser extent by other species such as Aedes albopictus, Aedes polynesiensis, Aedes scutellaris 1. Humans are the main reservoir and host causing global spread and therefore it has been a major public health concern, with an incidence increase of 30-fold in the last five decades 2. It was estimated from de 2013 Global Burden of Diseases (GBD) that, in that year, there were 58ยท40 million dengue cases in 141 countries, with a 18% hospital admission rate and over 13,000 deaths. The annual global cost with the disease was 8,9 billion dollars 3.
DF is a systemic and dynamic infection with a broad clinical spectrum of manifestations that may range from asymptomatic disease to serious and life-threatening hemorrhagic syndromes, known as dengue hemorrhagic fever (DHF), and dengue shock syndrome (DSS). Both these phases are considered complications, and uncomplicated cases are characterized by self-limited fever, lasting usually for 5โ€“7 days. Dengue can be debilitating during the acute illness stage and classical clinical features in adults include high fever (usually biphasic), severe headache, retroorbital pain, myalgia, arthralgia, nausea, vomiting, and petechiae. Leukopenia and thrombocytopenia are frequent findings2. No effective therapy is currently available and treatment is purely symptomatic, requiring a high level of patient care. Patients can be hospitalized to facilitate fluid replacement and blood transfusions, when indicated. Severe cases occur in approximately 500,000 people/year and present a mortality rate of up to 10% for hospitalized patients and 30% for non-hospitalized patients4.
A single-stranded RNA virus, DENV has a positive-sense genome, containing approximately 10,700 bases. This genome contains a single open reading frame (ORF) which, when cleaved, gives rise to three structural proteins, capsid [C], pre-membrane [prM], and envelope [E], and seven non-structural proteins (NS1, NS2A, NS2B, NS3, NS4A, NS4B, NS5) 5โ€“7. The various genotypes of DENV arise due to the action of an RNA polymerase that lacks proofreading activity, resulting in at least one new mutation being produced with each replication of its genome 7,8.
About 1,000 years ago, it is estimated that an infectious cycle between non-human primates and mosquitoes gave rise to the four serotypes of dengue virus as they are known today and they share approximately 65% amino acid sequence similarity. The first time the virus was isolated, in 1943 in Japan, was named DENV1 (with 5 genotypes) and this same serotype was reported in the Americas in 1977 and in Africa in 19848,9. Approximately 400โ€“600 years ago, DENV2 (with 5 genotypes) diverged from the sylvatic ancestor and was first isolated in Hawaii in 1945, in 1964 in Africa and 1953 in the Americas9,10. In 1956, DENV3 (with 4 genotypes) and DENV4 (with 4 genotypes) were first reported in Asia (Philippines and Thailand). DENV3 arrived in 1962 in Asia, in 1963 in the Americas and in 1984 in Africa. DENV4 had its report not as faithful as it happened with the other serotypes so, it was not reported until 1981 in Americas9,11,12.
These four serotypes are genetically similar and share approximately 65% of their genomes but each dengue virus serotype shows antigenic differences which often have spatial and temporal disjunct distributions. One genotype of one serotype can persist for many years in a given geographic region and then die out and even be replaced by a new genotype or lineage but still cause very similar disease13,14 in humans lineage replacement events had several explanations: a) the stochastic nature of DENV transmission; b)variations in conditioning within a population; c) increased viremia in the human host are cited as reasons for these antigenic differences; d) Co-circulation of multiple dengue serotypes, however, epidemiological studies have shown that immune enhancement is also a strong line of evidence 12,15,16.
The dengue fever is a serious public health problem in many countries around the world, and the lack of specific treatments and effective vaccines makes disease control more difficult. In addition, the lack of basic infrastructure in growing population areas, such as sanitation, garbage collection, water treatment, and sewage treatment, creates an environment conducive to the proliferation of the dengue mosquito. Although awareness campaigns, environmental cleanup and sanitation, and case monitoring can help reduce the incidence of the disease, ongoing research is essential to better understand the pathogenesis of the disease, the factors that affect the transmission of the virus, and how environmental factors can influence mosquito control. This research is crucial to develop more effective strategies for the prevention, diagnosis, and treatment of dengue 7,17,18.
The present study evaluated and reviewed the temporal spreading and evolution of dengue virus serotypes worldwide by Bayesian method evaluating 1,581 whole genome sequences (WGS) of dengue virus obtained between January 1944 to July 2022.