Abstract
The emergence of the Zika virus (ZIKV) mirrors its evolutionary nature and, thus, its ability to grow in diversity or complexity (i.e., related to genome, host response, environment changes, tropism, and pathogenicity), leading to it recently joining the circle of closed congenital pathogens. The causal relation of ZIKV to microcephaly is still a much-debated issue. The identification of outbreak foci being in certain endemic urban areas characterized by a high-density population emphasizes that mixed infections might spearhead the recent appearance of a wide range of diseases that were initially attributed to ZIKV. Globally, such coinfections may have both positive and negative effects on viral replication, tropism, host response, and the viral genome. In other words, the possibility of coinfection may necessitate revisiting what is considered to be known regarding the pathogenesis and epidemiology of ZIKV diseases. ZIKV viral coinfections are already being reported with other arboviruses (e.g., chikungunya virus (CHIKV) and dengue virus (DENV)) as well as congenital pathogens (e.g., human immunodeficiency virus (HIV) and cytomegalovirus (HCMV)). However, descriptions of human latent viruses and their impacts on ZIKV disease outcomes in hosts are currently lacking. This review proposes to select some interesting human latent viruses (i.e., herpes simplex virus 2 (HSV-2), Epstein–Barr virus (EBV), human herpesvirus 6 (HHV-6), human parvovirus B19 (B19V), and human papillomavirus (HPV)), whose virological features and co-exposition with ZIKV may provide evidence of the syndemism process, shedding some light on the emergence of the ZIKV-induced global congenital syndrome in South America.
Highlights
This review proposes to select some interesting human latent viruses (i.e., herpes simplex virus 2 (HSV-2), Epstein–Barr virus (EBV), human herpesvirus 6 (HHV-6), human parvovirus B19 (B19V), and human papillomavirus (HPV)), whose virological features and co-exposition with Zika virus (ZIKV) may provide evidence of the syndemism process, shedding some light on the emergence of the ZIKV-induced global congenital syndrome in South America
Microcephaly is a common feature of several congenital viruses (e.g., human cytomegalovirus (HCMV), herpes simplex virus (HSV), human immunodeficiency virus (HIV), and rubella virus); it could be caused by exposure to toxics
This study suggests an increase in cellular damage associated with ZIKV and the herpes virus family infection and/or in ZIKV facilitating the reactivity of other herpes viruses and neuronal injury by indirect mechanisms (Figure 5: Reactivation) [154]
Summary
A strange silent period of almost seven years (2007–2015) elapsed between the emergence of the Zika virus (ZIKV) in Oceania, defined by an increased incidence in the classical form of the illness, i.e., “Zika fever” (Yap in 2007: 49 confirmed cases and 39 probable cases), and the South American outbreak (Brazil in 2015: 440,000–1,500,000 reported cases), where the virus marked its re-emergence in powerful and serious forms with atypical clinical manifestations in humans, and shading the French Polynesian outbreak two years before (French Polynesia in 2013: 294 confirmed cases and approximately 8000–19,000 suspected cases) [1,2,3,4,5,6]. In light of global public health being in a state of high tension, this evidence has led to the declaration of ZIKV as a new congenital pathogen with potential risk of vertical transmission and association with specific fetal effects (such as microcephaly), referred to as CZS (e.g., in Brazil’s PAHO commitment (Pan American Health Organization), the World Health Organization’s 2015 report (WHO), and the WHO’s 2016 statement) This sudden attention might result in skews (both quantitative and qualitative) in the form of overestimating the number of ZIKV congenital infections and, by attributing an overly strong correlation between ZIKV and observed congenital manifestations influenced by confounding factors [29,30]. Campos et al proposed that “the unusual distribution of microcephaly in the Northeast region might be accentuated by prior, sequential exposition and/or co-viral infection with other pathogen”, suggesting that ZIKV is not the only culprit [55,56,57,58]
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