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23 November 2024: Review Articles  

A Review of Emerging Viral Pathogens and Current Concerns for Vertical Transmission of Infection

Dinah V. Parums1BDEF*

DOI: 10.12659/MSM.947335

Med Sci Monit 2024; 30:e947335

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Abstract

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ABSTRACT: Vertical transmission, or mother-to-child transmission, of bacterial, viral, or parasitic infection is rare due to the success of the barrier functions of the placental maternal-fetal interface, which provides physical, molecular, and immunological mechanisms to protect the developing fetus. Infections in pregnancy that can cross the placenta and reach the fetus can cause fetal loss, stillbirth, or prematurity or can lead to congenital infection, malformation of organs, and neonatal disease at birth. The acronym TORCH stands for Toxoplasma gondii, other, rubella, cytomegalovirus, and herpes simplex virus (HSV). Within the TORCH category of ‘other,’ there are increasing emerging viral pathogens that can pass from mother to fetus, including Ebola virus, Zika virus, and emerging arbovirus infections, including West Nile virus and Rift Valley fever virus. Although SARS-CoV-2 has rarely been reported to show transplacental spread, the recent COVID-19 pandemic has highlighted the importance of surveillance of new human pathogens with rapidly evolving transmission patterns. This article reviews the protective roles of the placental maternal-fetal interface, the concept of TORCH infections, and the emergence of viral pathogens currently causing concerns for vertical transmission from mother to fetus.

Keywords: review, vertical transmission, maternal infection, Fetal Infection, Emerging Viral Infection, TORCH Pathogens

Introduction

Vertical transmission, or mother-to-child transmission, of bacterial, viral, or parasitic infection is rare due to the success of the barrier functions of the placental maternal-fetal interface, which provides physical, molecular, and immunological mechanisms to protect the developing fetus [1,2]. Infections in pregnancy that cross the placenta can cause fetal loss, stillbirth, or prematurity or can lead to congenital infection, malformation of organs, and neonatal disease at birth [3,4]. The acronym TORCH, which stands for Toxoplasma gondii, other, rubella virus, cytomegalovirus, and herpes simplex virus, refers to pathogens that lead to congenital disease [5,6]. Within TORCH infections, the category of ‘other’ now includes several bacteria, viruses, and parasites that have developed mechanisms to bypass the placental maternal-fetal defense systems [6]. The list of infections that can be vertically transmitted is increasing with the inclusion of emerging infections (Table 1) [1,6].

Vertical transmission of pathogens across the placental maternal-fetal interface can result in teratogenic effects in the fetus, resulting in congenital anomalies [3,4]. Congenital abnormalities have been reported in up to 3% of live births, but the proportion attributable to vertically transmitted infection remains unclear [5]. Vertical transmission of infection can also result in growth restriction, miscarriage, stillbirth, prematurity, neonatal death, and maternal morbidity [3,4]. Vertical transmission of pathogens across the maternal-fetal interface that results in fetal infection can affect organogenesis, leading to congenital anomalies in any major organ system [3].

Pregnancy loss through miscarriage or stillbirth, which is intrauterine fetal death after 20 weeks of gestation, can also be caused by infection [5,7]. Between 10–30% of all stillbirths are reported to be caused by infection [5,7]. However, the low rates of diagnostic testing for infections in pregnant women will likely result in underestimating this association [4,5]. The rate of pregnancy loss varies due to several factors, including the specific pathogen and the fetal gestational age at infection [7]. The mechanisms of pregnancy loss associated with TORCH infections can be pathogen-mediated, placenta-mediated, or due to the effects of inflammation on inducing preterm delivery [8]. Several outcomes of congenital infection may not become manifest until after delivery, including neonatal hearing loss, blindness, and developmental delay [8].

Maternal infection, combined with the effects of infection and inflammation of the placental maternal-fetal interface, can cause preterm labor, resulting in a premature infant that suffers the sequelae of prematurity, with increased mortality and lifelong consequences that can affect all major organ systems [9,10]. Also, maternal infection is associated with fetal sepsis, which is an important cause of neonatal morbidity and mortality, particularly in premature or low birthweight infants [8]. This article aims to review the current status of established and emerging pathogens that show vertical transmission (TORCH pathogens) and the status of emerging pathogens of concern (Table 1) [1,6].

The Maternal-Fetal Interface and Defense from Infection

The placental maternal-fetal interface provides oxygen and nutrition to the developing fetus and protects the allogeneic fetus from immune-mediated attack and injury [2,11]. The placenta allows close contact between maternal and fetal cells at the maternal-fetal interface and regulates immune interactions between the mother and fetus [12]. Decidua, derived from the uterine endometrium, is located between the myometrium and the fetal membranes [11,12]. The placenta usually forms by the third week of gestation and consists of an external syncytiotrophoblast layer and an internal cytotrophoblast layer that functions as a significant barrier between the fetus and the mother [13].

Maternal leukocytes are recruited to the maternal-fetal interface by maternal cytokines and include decidual natural killer (NK) cells (70%), decidual macrophages that are antigen-presenting cells (APCs) (20%), and regulatory T cells (Tregs) (10%) [13]. Decidual macrophages include M1 and M2 macrophages that have a role in vascular remodeling and preventing infections from crossing the maternal-fetal interface [13]. As pregnancy progresses, the maternal immune response shifts towards Th2/antibody-mediated immunity rather than cell-mediated immunity by releasing anti-inflammatory cytokines, IL-4, IL-5, and IL-10, to protect the developing fetus [14]. Syncytiotrophoblast secretes interferon-gamma, immunoglobulin G (IgG) receptors, and Toll-like receptors (TLRs) [14,15]. Infection that involves the placenta may trigger the release of pro-inflammatory cytokines, including IL-6, IL-12, and TNF-alpha, which increase the risk of abortion, preterm labor, or maternal pre-eclampsia [15].

The placenta has important physical and immunological roles in fetal defense from infections. The integrity of the placental maternal-fetal interface is due to several unique properties of trophoblast. The external layer of the syncytiotrophoblast lacks cellular junctions and has a dense brush border at the apical surface that protects against infections, particularly from parasites [16]. The placenta secretes antiviral cytokines, including interferon-gamma, which is secreted by the syncytiotrophoblast [15]. TLRs expressed on trophoblast provide a first-line defense system against microbial transmission across the placenta and can recognize invasive pathogens and endogenous cell necrosis factors to link innate and adaptive immune responses [15]. From the second trimester of pregnancy, IgG receptors are increasingly expressed by the syncytiotrophoblast layer and actively transport protective maternal antibodies to the fetus [17].

TORCH Infections: Toxoplasmosis, Rubella, Cytomegalovirus (CMV), Herpes Simplex Virus (HSV)

The TORCH acronym is well-established and commonly used in maternal and perinatal medicine [1,6]. However, the list of – Other – infections is increasing as new infections that can be vertically transmitted continue to emerge (Table 1) [1,6]. Therefore, there have been recommendations to broaden or redefine the TORCH classification [18].

Toxoplasmosis, due to infection with the protozoan parasite Toxoplasma gondii, can cause symptomatic or asymptomatic congenital toxoplasmosis. Symptoms in the neonate include fever, seizures, a maculopapular rash, hepatosplenomegaly, or jaundice [19]. When undiagnosed in the neonate, long-term complications of toxoplasmosis include chorioretinitis and loss of vision, sensorineural hearing loss (SNHL), intellectual disability, cerebral palsy, and seizures with cerebral imaging that shows microcalcifications [19].

Congenital rubella syndrome (CRS) is rare in developed countries with rubella immunization programs. Infants with CRS can have a range of clinical manifestations of varying severity, including cataracts, SNHL, cardiac malformations, microcephaly, low birth weight, hepatosplenomegaly, jaundice, thrombocytopenia, purpuric skin lesions (extramedullary hematopoiesis) [20].

Because congenital cytomegalovirus (CMV) is ubiquitous, congenital CMV infection is the leading cause of nonhereditary SNHL in neonates [20]. However, it can also cause other long-term neurodevelopmental disabilities, including impaired vision, cerebral palsy, intellectual disability, and seizures [20]. Most infants with congenital CMV are asymptomatic, but approximately 10% may have SNHL identified by newborn hearing testing, growth retardation, microcephaly, skin petechiae, neonatal jaundice, hepatosplenomegaly, thrombocytopenia, chorioretinitis, and seizures [20]. Asymptomatic and symptomatic infants with congenital CMV have a significant risk of developing late complications, including SNHL, impaired vision, intellectual disability, and delayed motor development [20].

Most cases of neonatal HSV infection are acquired perinatally during birth, primarily through an infected maternal genital tract [21]. The infected newborn may show one of three infection patterns: localized infection of the eyes, mouth, and skin; localized CNS infection; and disseminated HSV infection. Congenital (in utero) HSV infection is rare and usually results from maternal viremia when the mother has a primary HSV viremia during pregnancy [21].

There is a lack of global consensus on current guidelines for maternal screening for TORCH infections during pregnancy [22,23]. The US Centers for Disease Control and Prevention (CDC) and the American College of Obstetricians and Gynecologists (ACOG) recommend that pregnant women should be screened for rubella and syphilis at the first prenatal visit [22,23]. However, in other countries, pregnant women may also be screened for toxoplasmosis [22,23]. Asymptomatic newborn infants are not usually screened for congenital infections, but some exceptions exist. In the US, infants who fail an audiometry test will be screened for CMV infection, and some US states and European countries have universal newborn screening for toxoplasmosis [24]. Routine screening of all pregnant women for the increasing range of TORCH infections is costly and lacks diagnostic accuracy [22]. Maternal infection risk factors and the presentation of TORCH infections may direct infection screening during antenatal maternal management [22].

Table 1 summarizes the current status of pathogens with vertical transmission, including TORCH infections [1,6]. The following is a review of the concerns regarding the effects of emerging viruses on the mother and fetus, including Ebola virus, Zika virus, and emerging arbovirus infections, including West Nile virus and Rift Valley fever virus, and the reasons why maternal surveillance for SARS-CoV-2 and its effects on pregnancy outcomes should continue.

Ebola Virus

The Ebola virus is an enveloped RNA virus belonging to the Filoviridae family, and is highly contagious with transmission by direct contact with the blood, organs, or bodily fluids of an infected person and transmission by contact with objects (fomites) [25]. Maternal Ebola virus infection results in widespread hemorrhage, preterm labor, miscarriage, and high maternal (85%) and fetal mortality (almost 100%) [25]. Reports from the 2013–16 Ebola outbreak in West Africa, pregnant women with viremia who survived Ebola virus disease delivered stillborn infants and had high viral RNA levels in placental and fetal swabs [25]. Studies have identified the Ebola virus in the placental syncytiotrophoblast [25].

Zika Virus

The Zika virus is an RNA virus of the Flaviviridae family [26,27]. The Zika virus has two modes of transmission to the mother, including vector-borne transmission by Aedes aegypti mosquitoes and vector-independent sexual transmission or by blood transfusion [26]. Vertical transmission to the fetus occurs in up to 10% of infected pregnant mothers [26]. Between 2013–14, outbreaks of maternal infection with Zika virus were reported in French Polynesia, with an outbreak of 2,000 reported cases in Brazil in 2015–16 [27]. Vertical transmission of the Zika virus resulted in congenital neonatal infection, with impaired neurodevelopment, microcephaly, ventriculomegaly, and developmental delays [27,28]. The discrepancy between fetal infection and the diverse neurological sequelae of disease has led to the separation of congenital Zika virus infection and congenital Zika virus syndrome [28].

The presentation of Zika virus infection in the mother occurs between 3–14 days after viral exposure and lasts for less than a week and includes conjunctivitis, a maculopapular rash, arthralgia, and fever (37.8–38.5°C) [28]. Outbreaks of cases of Zika virus congenital disease occur in waves, which suggests that immunity is important for regulating Zika virus infection of the maternal host [27]. Zika virus infection in the first trimester has the highest risk of vertical transmission [27]. Unlike other TORCH pathogens, the mechanisms used by the Zika virus to cross the placental barrier remain unknown [27]. However, pre-existing dengue virus immunity is associated with a reduced risk of Zika virus infection [29].

In the US, diagnostic guidelines have recommended screening of pregnant women with a history of travel to endemic areas or other risks for exposure [26]. Laboratory testing requires nucleic acid amplification testing [NAAT] and testing for IgM [26]. In screened-positive pregnant women, fetal imaging with ultrasonography (for microcephaly and complex brain malformations) is advised [26]. However, persistent maternal viremia has been reported, possibly due to viral replication in the fetus or placenta and transmission to maternal blood [30]. The true rate of asymptomatic Zika virus infection is unknown but is probably high, as approximately 20% of infected individuals are symptomatic [30,31]. It is also possible that the role of vertical transmission of Zika virus infection as a cause of congenital birth defects has been underestimated for decades [31].

Emerging Arbovirus Infections, Including West Nile Virus and Rift Valley Fever Virus

West Nile virus is an arthropod-borne flavivirus that targets the neurological system [32]. Vertical transmission of West Nile virus has been reported and results in fetal and neonatal central nervous system (CNS) abnormalities that include hydrocephalus and microcephaly [32]. Rift Valley fever virus is an arbovirus in the Bunyaviridae family, transmitted by an arthropod vector and associated with severe disease in domesticated animals and livestock [33]. In domesticated animals, Rift Valley fever virus outbreaks result in fetal loss and stillbirth in up to 100% of pregnant animals [33]. In humans, although maternal infection is rare, vertical transmission can occur in the third trimester of pregnancy and results in increased rates of miscarriage [33]. In vitro culture of human placental trophoblast has demonstrated viral replication in cytotrophoblast and syncytiotrophoblast [33]. Other arboviruses that can replicate successfully in human trophoblast in vitro include Chikungunya, Mayaro, and Powassan virus, neurotropic viruses with the potential for vertical transmission [33].

Zika virus outbreaks have raised awareness of mosquito-borne arbovirus diseases, which are now a global concern due to awareness of their effects on maternal, neonatal, and child health, particularly in developing countries [34,35]. Climate change, international travel, and increasing urbanization allow arboviruses to spread to new populations, including pregnant women [36]. Clinical and preclinical studies have shown that arboviruses can infect the nervous system, major organs, and placenta [34,35]. Emergent and re-emergent arbovirus infections can result in fetal loss, obstetric complications, and congenital abnormalities in the fetus [34]. Worldwide, more than 100 arbovirus species can cause human disease, but only 500 arboviruses have been identified, raising concerns for future emergent viral pathogens [36]. In healthy adults, arbovirus infections are often asymptomatic or minimally symptomatic in the healthy adult population, but some arboviruses are of concern in pregnant women [36]. These concerns were recognized by the WHO on March 22, 2022, with the launch of the Global Arbovirus Initiative to begin to provide consensus guidelines for infection surveillance and prevention of vertical viral transmission in pregnant women and to identify emerging infections [35].

SARS-CoV-2 Infection and COVID-19

During the first year of the COVID-19 pandemic, there were concerns regarding the effects of SARS-CoV-2 infection in pregnant women and the possibility of vertical transmission to the fetus [37]. These concerns resulted in public health initiatives encouraging pregnant women to ensure their vaccination status was current [38]. However, studies have shown a very low rate of transplacental SARS-CoV-2 transmission of <1% [39]. Maternal antibody transfer to the fetus does occur and is more efficient if maternal infection with SARS-CoV-2 occurs during the first or second trimester of pregnancy [39].

However, SARS-CoV-2 has shown rapid development of mutational variants with increased levels of infectivity and different transmission patterns [40]. In February 2024. Reeves and colleagues reported the findings from a retrospective cohort study that included outcomes from 57,563 women with confirmed SARS-CoV-2 infection in pregnancy, reported to the Surveillance for Emerging Threats to Pregnant People and Infants Network, which involved six US jurisdictions [38]. Data collection included positive polymerase chain reaction (PCR) tests for SARS-CoV-2, birth certificate data, immunization records, and fetal death records [38]. Cases of spontaneous abortion (<20 weeks of gestation), stillbirth (≥20 weeks of gestation), preterm birth (<37 weeks of gestation), small for gestational age, and term infant neonatal intensive care unit (NICU) admissions were identified [38]. The authors compared two periods, before and after the predominance of the Delta variant of SARS-CoV-2, between March to June 2020 and June to December 2021 [38]. Of 57,563 pregnancy outcomes, 99.3% (57,188) were live births, 0.1% (65) were spontaneous abortions, and 0.5% (310) were stillbirths [38]. However, in 2020 and 2021, most pregnant women were unvaccinated at the time of SARS-CoV-2 infection and would have been expected to have more severe COVID-19 symptoms [38]. Although there is no evidence to support current concerns for vertical transmission of SARS-CoV-2, this is a virus with a high mutation rate and changing patterns of transmission, which highlights the importance of continued infection surveillance and implementation of immunization programs, including in pregnant women [40].

An outcome of the recent COVID-19 pandemic was to highlight the health of women during pregnancy [41]. Some women infected with SARS-CoV-2 during pregnancy have shown the presence of the virus in the syncytiotrophoblast [41]. However, the placenta retains its barrier function even during severe maternal infection [41]. The risk to the fetus of vertical transmission of SARS-CoV-2 is minimal, and there is no evidence that SARS-CoV-2 is teratogenic. However, COVID-19 during pregnancy increases the risk of maternal mortality and pregnancy complications, particularly in the third trimester [41]. Therefore, women who intend to become pregnant or who are pregnant should be encouraged to ensure they are fully vaccinated to protect them from severe maternal COVID-19.

Conclusions

Infectious disease surveillance, particularly of emerging human pathogens, requires recognizing the potential for vertical transmission, the effects on the mother, fetus, and neonates, and potential long-term consequences for human health. Infection surveillance and increased understanding of the pathogenesis and modes of transmission of emerging viruses, including Ebola virus, Zika virus, and arthropod-borne viruses, including West Nile virus and Rift Valley fever virus, have raised concerns regarding the implications of undetected infections and their consequences. In the years since the COVID-19 pandemic, the high mutation rate of SARS-CoV-2 has resulted in viral variants with changes in infectivity and transmission rates of this virus, which adversely affects maternal health and requires continued surveillance of SARS-CoV-2 variants and their effects on pregnancy outcomes.

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