Presence of entry receptors and viral markers suggest a low level of placental replication of hepatitis B virus in a proportion of pregnant women infected with chronic hepatitis B

Garg, Garima; Meenu, M. N.; Patel, Kajal; Singh, Ravinder J.; Gupta, Priyal; Purwar, Shashank; Mukhopadhyay, Sabyasachi; Mishra, Nitu; Gupta, Sudheer; Rawat, Sumit Kumar; Goel, Harsh; Kumar, Rahul; Tanwar, Pranay; Singh, Rajesh; Nema, Shashwati; Biswas, Debasis; Trehanpati, Nirupma; Singh, Anirudh; Vyas, Ashish Kumar

doi:10.1038/s41598-022-22699-8

Cited by 4 publications

(3 citation statements)

References 28 publications

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“…Several routes of the vertical transmission of pathogens across the maternal–fetal interface are known to occur, including direct transplacental transmission, placental disruption, fetal–maternal hemorrhage, transmission across fetal membranes, and ascending infections [ 38 , 39 ]. The presence of viral components in the placenta may be due to the translocation of viral components from peripheral blood or viral replication in the placenta [ 40 ]. We previously showed that BPVs have the potential to replicate in the placenta as we detected BPV L1 expression in the binucleate trophoblast cells of the placenta from pregnant cows [ 15 ].…”

Section: Discussionmentioning

confidence: 99%

Vertical Intrauterine Bovine and Ovine Papillomavirus Coinfection in Pregnant Cows

De Falco,

Cutarelli,

Leonardi

et al. 2024

Pathogens

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There is very little information available about transplacental infections by the papillomavirus in ruminants. However, recent evidence has emerged of the first report of vertical infections of bovine papillomavirus (BPV) in fetuses from naturally infected, pregnant cows. This study reports the coinfection of BPV and ovine papillomavirus (OaPV) in bovine fetuses from infected pregnant cows suffering from bladder tumors caused by simultaneous, persistent viral infections. Some molecular mechanisms involving the binary complex composed of Eras and platelet-derived growth factor β receptor (PDGFβR), by which BPVs and OaPVs contribute to reproductive disorders, have been investigated. A droplet digital polymerase chain reaction (ddPCR) was used to detect and quantify the nucleic acids of the BPVs of the Deltapapillomavirus genus (BPV1, BPV2, BPV13, and BPV14) and OaPVs belonging to the Deltapapillomavirus (OaPV1, OaPV2, and OaPV4) and Dyokappapapillomavirus (OaPV3) genera in the placenta and fetal organs (heart, lung, liver, and kidneys) of four bovine fetuses from four pregnant cows with neoplasia of the urinary bladder. A papillomaviral evaluation was also performed on the bladder tumors and peripheral blood of these pregnant cows. In all fetal and maternal samples, the genotype distribution of BPVs and OaPVs were evaluated using both their DNA and RNA. A BPV and OaPV coinfection was seen in bladder tumors, whereas only BPV infection was found in peripheral blood. The genotype distribution of both the BPVs and OaPVs detected in placentas and fetal organs indicated a stronger concordance with the viral genotypes detected in bladder tumors rather than in peripheral blood. This suggests that the viruses found in placentas and fetuses may have originated from infected bladders. Our study highlights the likelihood of vertical infections with BPVs and OaPVs and emphasizes the importance of gaining further insights into the mechanisms and consequences of this exposure. This study warrants further research as adverse pregnancy outcomes are a major source of economic losses in cattle breeding.

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Section: Discussionmentioning

confidence: 99%

Vertical Intrauterine Bovine and Ovine Papillomavirus Coinfection in Pregnant Cows

De Falco,

Cutarelli,

Leonardi

et al. 2024

Pathogens

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“…Inappropriate trophoblastic invasion and immune response could promote dysfunction of the placenta and alter the blood flow to the fetus, 22 while interruption of blood supply to fetus is associated with ACC. As HBV biomarkers could be detected in the placenta, 23 , 24 another possible pathogenic mechanism could involve maternally generated antibodies to HBsAg, PreS1, or PreS2, and the corresponding antigens that form circulating complexes. These complexes could deposit in the capillaries of the placenta and cause thrombotic events that might disrupt skin development in the fetus.…”

Section: Discussionmentioning

confidence: 99%

Type VII Aplasia Cutis Congenita in Neonates Related to Maternal HBV Infection? Case Report and Literature Review

Li¹,

Zhang²,

Yang³

et al. 2023

CCID

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Aplasia cutis congenita (ACC) is a rare disease with an unclear pathogenic mechanism. ACC has been suggested to result from the disrupted development or degeneration of skin in the uterus. This study describes two cases that may have underlying pathogenic cause that have not been previously reported. Two neonates who were admitted to the neonatal intensive care unit due to “skin lesions on the limbs” without other deformities or complications were diagnosed with type VII ACC by dermatologist. The mothers showed positivity for hepatitis B virus (HBV) surface antigen and elevated level of HBV DNA copies, which may be related to ACC. But this association could be a coincidence. Both neonates were treated with antibacterial dressings and achieved satisfactory healing.

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“…Garima et al. ( 57 ) also observed that even at relatively low levels, receptors and HBV markers could replicate in the placenta. As the placenta developed, trophoblast cells differentiated and fused into multinucleated cells that formed the syncytiotrophoblast, and the maturity of the placenta and specific maternal antibodies, such as maternal immunoglobulin G (IgG), had the ability to reduce the risk of HBV transmission ( 55 ).…”

Section: T Cells and Hbv Infectionmentioning

confidence: 98%

Effects of hepatitis B virus infection and strategies for preventing mother-to-child transmission on maternal and fetal T-cell immunity

Cao

Zhang

et al. 2023

Front. Immunol.

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One of the most common routes of chronic hepatitis B virus (HBV) infection is mother-to-child transmission (MTCT). Approximately 6.4 million children under the age of five have chronic HBV infections worldwide. HBV DNA high level, HBeAg positivity, placental barrier failure, and immaturity of the fetal immune are the possible causes of chronic HBV infection. The passive-active immune program for children, which consists of the hepatitis B vaccine and hepatitis B immunoglobulin, and antiviral therapy for pregnant women who have a high HBV DNA load (greater than 2 × 105 IU/ml), are currently two of the most important ways to prevent the transmission of HBV from mother to child. Unfortunately, some infants still have chronic HBV infections. Some studies have also found that some supplementation during pregnancy can increase cytokine levels and then affect the level of HBsAb in infants. For example, IL-4 can mediate the beneficial effect on infants’ HBsAb levels when maternal folic acid supplementation. In addition, new research has indicated that HBV infection in the mother may also be linked to unfavorable outcomes such as gestational diabetes mellitus, intrahepatic cholestasis of pregnancy, and premature rupture of membranes. The changes in the immune environment during pregnancy and the hepatotropic nature of HBV may be the main reasons for the adverse maternal outcomes. It is interesting to note that after delivery, the women who had a chronic HBV infection may spontaneously achieve HBeAg seroconversion and HBsAg seroclearance. The maternal and fetal T-cell immunity in HBV infection is important because adaptive immune responses, especially virus-specific CD8 T-cell responses, are largely responsible for viral clearance and disease pathogenesis during HBV infection. Meanwhile, HBV humoral and T-cell responses are important for the durability of protection after fetal vaccination. This article reviews the literature on immunological characteristics of chronic HBV-infected patients during pregnancy and postpartum, blocking mother-to-child transmissions and related immune mechanisms, hoping to provide new insights for the prevention of HBV MTCT and antiviral intervention during pregnancy and postpartum.

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Presence of entry receptors and viral markers suggest a low level of placental replication of hepatitis B virus in a proportion of pregnant women infected with chronic hepatitis B

Cited by 4 publications

References 28 publications

Vertical Intrauterine Bovine and Ovine Papillomavirus Coinfection in Pregnant Cows

Vertical Intrauterine Bovine and Ovine Papillomavirus Coinfection in Pregnant Cows

Type VII Aplasia Cutis Congenita in Neonates Related to Maternal HBV Infection? Case Report and Literature Review

Effects of hepatitis B virus infection and strategies for preventing mother-to-child transmission on maternal and fetal T-cell immunity

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