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 Table of Contents  
Year : 2021  |  Volume : 5  |  Issue : 2  |  Page : 131-138

Dynamic immune status of pregnancy and dermatological diseases: An interplay

Department of Dermatology, Shri B.M. Patil Medical College, Hospital and Research Centre, BLDE (DU), Bijapur, Karnataka, India

Date of Submission05-Dec-2019
Date of Decision16-Feb-2020
Date of Acceptance26-Mar-2020
Date of Web Publication26-Aug-2021

Correspondence Address:
Arun C Inamadar
Department of Dermatology, Shri B.M. Patil Medical College, Hospital and Research Centre, BLDE (DU), Bijapur - 586 103, Karnataka
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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/CDR.CDR_47_19

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Dynamic changes of immune system in the various stages of pregnancy affect the course of various diseases afflicting the mother alongside determining how pregnancy affects these diseases. To understand this, a thorough knowledge on how the immune system differs in pregnancy is essential. The complex interplay between the maternal and fetal immune systems via placenta in order to maintain the pregnancy leads to waxing and waning of immune responses in both mother and fetus. This dynamic nature of immune responses can heavily influence the manifestations and severity of several dermatological diseases, whether infectious or noninfectious. Here, we discuss the effect of altered immunity of gestation on a few important dermatological diseases such as psoriasis, systemic lupus erythematosus, syphilis, varicella, leprosy, and TORCH infections and vice versa.

Keywords: Immune system, leprosy, pregnancy, psoriasis, syphilis, systemic lupus erythematosus, TORCH infections, varicella

How to cite this article:
Parthasarathy N, Janagond AB, Inamadar AC, Lingaiah A, Gangadhar M, Arsiwala NZ, George RM, Ratan V. Dynamic immune status of pregnancy and dermatological diseases: An interplay. Clin Dermatol Rev 2021;5:131-8

How to cite this URL:
Parthasarathy N, Janagond AB, Inamadar AC, Lingaiah A, Gangadhar M, Arsiwala NZ, George RM, Ratan V. Dynamic immune status of pregnancy and dermatological diseases: An interplay. Clin Dermatol Rev [serial online] 2021 [cited 2022 May 17];5:131-8. Available from: https://www.cdriadvlkn.org/text.asp?2021/5/2/131/324562

  Introduction Top

Human immunity is a complex system which is influenced by a wide array of factors. The course of various infectious and noninfectious dermatological conditions is altered depending on individual immunological status and multiple factors affecting it.

Pregnancy is an essential and the most important event in the conservation of species. To aid this process, the immune system changes dynamically in the various stages of pregnancy. This change in turn affects the course of various diseases afflicting the mother alongside determining how pregnancy affects these diseases. To understand this complex process of the effect of pregnancy on diseases and vice versa, a thorough knowledge on how the immune system differs in pregnancy is essential.[1]

Previously, pregnancy was thought to be a state of immunosuppression, but, now, it is considered as a unique immune condition in which the immunity is modulated and not merely suppressed.[1] Human placenta also plays an important role in changing and adapting the maternal immune system to pregnancy. Therefore, pregnant women are indeed capable of having vigorous immune responses when there is a risk to mother and/or fetus.[2]

Immune framework during pregnancy

Because 50% of fetal genetic composition is derived from the father, the fetus which is similar to a transplanted organ is at a risk of being rejected by the immune system of the mother. These fetal antigens are tolerated by the maternal immune system by the suppression of cell-mediated immunity (CMI), while the humoral immunity is maintained normally. These changes take place at the maternal–fetal interface.[3] Immune framework during pregnancy is the consequence of an amalgamation of signals and responses from both mother's and fetoplacental immune system.[1]

Maternal–fetal interface

The interface between the mother and fetus is formed by the placenta and membranes of the fetus, i.e., amnion and chorion. On the fetal side of the interface, fetal syncytiotrophoblast, a specialized epithelium in the placenta, is responsible for exchanging nutrients by being directly in contact with the maternal blood. On the maternal side of the interface, the decidua is rich in immune cells such as regulatory T cells (Treg), macrophages, and uterine natural killer (uNK) cells.[1] These immune cells play an important role in implantation, placental development, and immunity against infectious diseases. uNK cells comprise 70% of the decidual leukocytes, while macrophages and dendritic cells account for 20%–25% and 1.7%, respectively. T cells contribute to 10%–20% of decidual leukocytes. However, B lymphocytes are very rarely present in the decidua. uNK cells have weak cytotoxic property and do not destroy trophoblasts.[4]

Trophoblasts identify microorganisms and induce immunity. Along with this function, they also have a role in the production of antimicrobial peptides such as human beta defensins 1 and 3, whose expression is regulated by trophoblastic toll-like receptor (TLR)-3, TLR-7, TLR-8, and TLR-9. Trophoblasts also express secretory leukocyte protease inhibitor, which is a powerful human immunodeficiency virus (HIV) inhibitor and bacterial lysis inducer.[1]

Fetal membranes express human leukocyte antigens (HLAs) which have tolerogenic properties rather than immunogenic ones. Major histocompatibility complex expression on trophoblasts is repressed, which is responsible for overcoming recognition and destruction by maternal immune cells.[4] Lack of HLA Class I expression by villous trophoblasts and HLA-A/HLA-B expression by extravillous trophoblasts, aids the evasion of maternal CD8+ T cell response.[5]

Earlier, gestation was viewed upon as a single event. However, realistically, it comprises of three distinctive phases of immunology exhibiting the following characteristic biological processes:[1]

  1. During implantation, the blastocyst breaks through the uterine epithelium and further invades the endometrium by damaging it. Subsequently, the trophoblast replaces the endothelium and vascular smooth muscle of the uterus, which helps in procuring a sufficient blood supply for the placenta and fetus. In order to satisfactorily repair the epithelial lining of the uterus and clear the remnants of the cells, an inflammatory environment is established. Therefore, the first trimester of pregnancy is a pro-inflammatory stage
  2. During the next immunological period, prompt growth and development of the fetus is observed. Due to the induction of an anti-inflammatory state, the maternal, placental, and fetal tissues exist in symbiosis
  3. In the final immunological period of gestation, complete fetal development is attained and the baby has to be delivered into the outer world. To facilitate this process, immune cells invade myometrium and promote reactivation of inflammation. This inflammatory state leads to uterine contraction, causing the baby to be expelled and placenta to be rejected.

To summarize, majority of the 1st trimester and nearing the completion of pregnancy are essentially pro-inflammatory, whereas, 2nd trimester and part of 3rd trimester are anti-inflammatory in nature.[2]

Although the immune system of the mother is continuously exposed to the fetal antigens, the fetus is tolerated by the mother's immune system by virtue of the following factors:[3]

  1. Humoral immunity: [Figure 1][3] shows the mechanism of humoral immunity. This immunity is responsible for regulating extracellular pathogens. T-helper type II (Th2) lymphocytes further enhance this immune response by co-stimulating, and thereby, inducing B-lymphocyte replication. Therefore, Th2 response plays an important role during gestation via robust antibody production against pathogens[3]
  2. CMI: This immune response is important for controlling intracellular pathogens. It differs from antibody-mediated immunity in being incited by T-helper type I (Th1) lymphocytes, which results in a release of different cytokines. Antigens present on cells infected by virus or other intracellular pathogens are recognized by the cytotoxic T cells, the chief effector cells in CMI, leading to the destruction of the affected cells[3]
  3. T-Helper cells and Th1–Th2 shift: The occurrence of Th1- or Th2-cell response depends on the cytokine background and co-stimulatory signals occurring at the time when T-helper cells are being activated along with various other elements.
Figure 1: Humoral immunity

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It is proposed that macrophages residing at the maternal–placental interface liberate cytokines which chiefly stimulate Th2 cells. This, along with hormonal changes altering the Th1–Th2 balance, causes a predominance of antibody-mediated immunity during pregnancy. Th2 cytokines cause a suppression of cytotoxic T cells, which leads to weakening of the CMI. On the other hand, the presence of Th2 cells in the decidual lining of uterus is responsible for the activation of B cells, resulting in antibody production, and thereby, suppression of CMI. This event is known as the Th1–Th2 shift of pregnancy.[3] Estradiol, progesterone, prostaglandin D2, and leukemic inhibitory factor, which are produced during pregnancy, support Th2 profile:[4]

  1. Systemic immune changes: Shifting of the immune response from Th1 type to Th2 type also has an impact on the maternal systemic immunity during the course of pregnancy. Because cell-mediated immune response is responsible for regulating intracellular offending agents, systemic suppression of this immunity may lead to increased susceptibility to some of these pathogens during gestation.[3]

Fetal inflammatory response syndrome

Certain placental viral infections trigger mild inflammation leading to the activation of maternal as well as fetal immunity. This event has various effects:[2]

  • Primarily, it can stimulate inflammatory reaction in fetus, without viral transmission to the fetus. This state is known as fetal inflammatory response syndrome which is characterized by the excessive amount of mediators of inflammation, such as interleukin (IL)-1, IL-6, IL-8, and tumor necrosis factor-alpha (TNF-α) in the placenta. However, no microorganisms are observed on cultivation. These mediators have an impact on the central nervous system (CNS) and cardiovascular system of the growing fetus
  • Secondarily, it sensitizes the mother to concurrent infection with bacteria and other microorganisms, thereby increasing the risk of infection.

To sum up, the complex interplay between the maternal and fetal immune systems via placenta in order to maintain the pregnancy leads to waxing and waning of immune responses in both the mother and the fetus. This dynamic nature of immune responses can heavily influence the manifestations and severity of several dermatological diseases, whether infectious or noninfectious. In this article, we aim to briefly discuss the effect of altered immunity of gestation on a few important dermatological diseases and vice versa.

Psoriasis and pregnancy

Psoriasis is a Th-1-mediated inflammatory disease that affects women in reproductive age group. A pregnant woman with psoriasis is at a higher risk of developing complications such as preterm labor and low-birthweight baby. Inflammation due to psoriasis can be associated with adverse outcomes in pregnancy. Pro-inflammatory cytokines such as IL-6, C-reactive protein, and TNF-α are increased during active psoriasis in both maternal serum and cord blood.[6] The various effects of psoriasis on pregnancy include gestational diabetes, gestational hypertension, antenatal hemorrhage, pre-eclampsia, and venous thromboembolism.[7],[8] A direct relation is observed between the severity of psoriasis and complications such as spontaneous abortions, preterm labor, stillbirth, and intrauterine growth restriction (IUGR).[8]

The effects of pregnancy on psoriasis can be varied. Most studies have shown that worsening of psoriasis during pregnancy occurs in 25%, improvement is seen in 50%, while there is no change in 25% of patients.[9] Appearance of new lesions of psoriasis is more frequent during the early postpartum period. Patients in whom psoriasis improves in first pregnancy, show similar response in subsequent pregnancies.[10] During pregnancy, there is Th-2 cytokine-mediated downregulation of immune response, which creates an anti-inflammatory state, thus antagonizing the effects of Th-1 cytokine and improving psoriasis. High levels of estrogen improve psoriasis, whereas progesterone has no effect on psoriasis.[11] A significant remission rate of psoriasis has been described in women who are HLA-Cw*0602 positive, while those negative for this allele show no change or worsening of the condition. This indicates that genetics may play a role in the improvement of psoriasis in pregnancy.[12]

Systemic lupus erythematosus and pregnancy

Fertility is generally not reduced in women with systemic lupus erythematosus (SLE) unless there is end-stage renal failure (chronic kidney disease Stage 5) associated with lupus nephritis, which can cause amenorrhea.[13] In other words, fertility is normal if renal function is good. Active lupus nephritis poses a significant risk to pregnancy and leads to 8%–36% of nonelective pregnancy loss.[14] Increased risk of spontaneous abortion, intrauterine death, preeclampsia, intrauterine growth retardation, and preterm birth are observed in pregnant women affected with SLE.[12] Presence of anti-Ro/La and antiphospholipid antibodies is associated with an increased incidence of fetal heart block and neonatal lupus.[13] Repeated abortions is an important complication of anti-phospholipid antibody syndrome.[15]

An increased risk of flares of SLE is seen during pregnancy and postpartum period (up to 3 months) as compared to nonpregnant patients.[16] Flares are uncommon especially if the patient is already on immunosuppressive therapy.[15] Patients on hydroxychloroquine show reduction in flares in pregnancy or during postpartum period, and discontinuation of drug results in increased disease activity.[16] Clinical remission or minimal lupus activity for 6 months before conception reduces the incidence of flares.[13]

Syphilis and pregnancy

According to the World Health Organization, syphilis harmfully affects 1,000,000 pregnancies yearly.[17] Maternal transmission of syphilis infection can occur either due to transmission of treponemes through placenta or through contact of baby with the lesion over the mother's genitalia during delivery.[18] Formerly, it was believed that spirochetes do not cross the placental membranes before 20 weeks of gestation. However, studies have shown the presence of these pathogens in the fetus as early as 9 weeks of gestation.[19] Delayed-type hypersensitivity (DTH) mediated by CD4+ T-cells is of particular importance in syphilis. Secondary and tertiary diseases follow if DTH response is ineffective. Whereas, CD8+ T-cell-mediated humoral antibody is relatively ineffective in controlling the progression of lesions or clearing the infection.[20]

The risk of infection being transmitted to the offspring decreases as the stage of maternal syphilis progresses. Around 70%–100% risk of transmission is seen in primary syphilitic stage, 40% during early latent stage, and is almost nil in the late latent stage.[17],[19] This is because the transmission is reliant on the spirochetes' levels in the mother's blood.[19]

Friability and hyperemia occurring in the pregnant cervix may provide access for the entrance of Treponema pallidum; nonetheless, pregnancy has no appreciated impact on syphilis.[17] However, untreated syphilitic infection occurring in pregnant women may have adverse effects on pregnancy such as spontaneous abortion, nonimmune hydrops, stillbirth, IUGR, prematurity, perinatal death of the fetus, and congenital syphilis in the newborn child.[18]

Congenital syphilis is classified into two phases: early congenital syphilis (manifests before 2 years of age) and late congenital syphilis (clinical manifestations occur after the age of 2 years).[17] Skin lesions observed are maculopapular rash and vesiculobullous eruptions, especially over the palms and soles. Deeply fissured papules can be seen at the angle of the mouth or lateral to the external nares. Anal condolymata and paronychia are also seen. Lesions over the lips, nostrils, and anus heal to form radiating scars (rhagades).[21]

Varicella and pregnancy

Varicella, commonly known as chicken pox, is an infection by varicella zoster virus which generally confers lasting immunity. Secondary attacks are uncommon, especially in immunocompetent individuals. Women who reach their childbearing age without developing immunity to varicella have a minor risk of developing chicken pox during pregnancy (0.05%–0.07%).[22] More severe disease is associated with primary varicella infection in pregnancy than reactivation. Effects on the fetus are worse if infection occurs early in pregnancy.[4]

Humans are the only source, and entry of virus into the host occurs through the conjunctiva and mucous membranes of the nasopharynx. At the end of the second viraemic phase, prodromal symptoms, such as headache, fever, and malaise, generally occur. This is followed by pruritus and maculopapular rash, which become vesicular before crusting about 5 days later. The patient is contagious from 2 days prior to the development of the rash until crusting of the vesicles.[23]

Maternal varicella is associated with greater risk for varicella pneumonia having a severe course, whereas fetal risk is associated with congenital varicella syndrome and neonatal varicella.[24]

The effects of varicella on pregnancy are enumerated in [Table 1].
Table 1: Effects of varicella on pregnancy[16],[17]

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Pregnancy increases the risk of developing varicella pneumonia along with an increase in general severity of the varicella infection itself. The risk of pneumonia increases with increasing gestational age.[23]

The incidence of maternal varicella pneumonia is 0.7–3 per 1000 pregnancies, and 10%–20% of chickenpox in pregnancy is complicated by maternal varicella pneumonia.[23]

Leprosy and pregnancy

Leprosy runs an altered course due to altered immunological response, nutritional changes, and increased secretion of steroids in pregnancy.[25] These changes occurring during gestation result in the depression of CMI, which in turn leads to an increase in the bacillary load. The increase in Bacillary Index is maximum in the third trimester and declines to prepregnancy levels during lactation wherein the CMI is restored. The age group with the highest incidence of pregnancy–leprosy association has been found to be 20–39 years.[26]

Around 20%–30% of females incubating the infection develop the signs and symptoms of leprosy for the first time in pregnancy.[26] Leprosy aggravates during pregnancy, i.e., downgrades toward lepromatous spectrum with appearance of new skin lesions and progressive nerve function impairment.[26] Multiplication of persisters due to suppressed CMI, especially during the third trimester, can end up in pregnancy-associated relapse of leprosy.[27] Reversal reactions are less frequent during pregnancy and present predominantly with cutaneous manifestations rather than neuritis.[25] Whereas, Type 2 reaction peaks in the third trimester, and is more severe and recurrent. Here, neurological damage occurs earlier than in nonpregnant women and can lead to permanent nerve damage.[26] During Type 2 reaction, neuritis affects almost 50% of pregnant women, mostly as silent neuritis with loss of both sensory and motor functions associated with the reaction.[26]

Leprosy is known to have only meager effects on the course of pregnancy, as opposed to the marked effect pregnancy has on the course of leprosy.[27] The manifestations are most pronounced in pregnant females with lepromatous leprosy. Children born to leprous mothers have been known to develop lesions of leprosy in the first few months after birth, due to transplacental infection with Mycobacterium leprae. The placental weight and placental coefficient have been found to be comparatively lower in women with leprosy.[26] Increased incidence of fetal loss, premature birth, low-birthweight baby, and intrauterine growth retardation have been observed in pregnant leprous women, which are attributed to fetoplacental inadequacy due to decreased uteroplacental perfusion.[27] The newborns of mothers on multidrug therapy may present with exfoliative dermatitis in the first few hours of life or develop hemolytic anemia later in life due to dapsone. Brownish discoloration of skin due to clofazamine impregnation into the skin is also observed.[25] The skeletal growth spurt during puberty and menarche for girls born to mothers with leprosy was observed to be significantly delayed.[26]

TORCH infections and pregnancy

The term TORCH stands for Toxoplasmosis, Others, Rubella, Cytomegalovirus (CMV), herpes simplex virus (HSV). The acronym TORCH originally consisted Toxoplasmosis, Rubella, CMV, and HSV. It was later expanded to include hepatitis viruses, HIV, and other infections such as Varicella and Parvovirus B19 under “others.”[28],[29] These infections contribute to a great extent of prenatal and infant morbidity and mortality.[28]


Transplacental transmission of Toxoplasma gondii following maternal primary infection during pregnancy, when there is high parasite burden with tachyzoites, results in congenital infection of the fetus. Persistent parasitemia due to infection of the mother around 3 months before conception may also transmit T. gondii, which extrapolates into the pregnancy.[28] Seroconversion occurring at 24–30 weeks of gestation poses the greatest risk of giving birth to a baby with symptomatic congenital toxoplasmosis (about 10%).[28]

The clinical signs and symptoms of congenital toxoplasmosis, if present, are often not recognized at birth, as sequelae usually develop later in life. The classical diagnostic triad of symptoms (chorioretinitis, hydrocephalus, and intracranial calcifications) is infrequently observed, but still remains highly indicative. More common features of presentation include anemia, seizures, jaundice, splenomegaly, hepatomegaly, and thrombocytopenia.[28] Cutaneous features are nonspecific such as maculopapular rash, petechiae, and ecchymoses; vascular lesions simulating “blueberry muffin;” and calcifications involving any part of the body.[30]

Many congenital manifestations of toxoplasmosis are similar to those seen in other TORCH infections. Infection occurring early in pregnancy presents with more severe features, whereas those occurring during the third trimester are commonly subclinical at birth.[28]

Newborns will still be at a high risk of developing late manifestations and sequelae of the infection even if they show mild or no features of infection at birth. These manifestations and sequelae include mental retardation, microcephaly, seizures, motor and cerebellar dysfunction, chorioretinitis, and sensorineural hearing loss (SNHL).[28]


Approximately 80%–100% of congenital rubella occurs primarily after maternal infection during the first trimester.[28] The most severe manifestations follow infection during this period. The risk of transmission decreases to 10%–20% during the second trimester, while at term again, there is an increase in the risk (around 60%).[28] Infection leads to miscarriage, stillbirth, or congenital rubella syndrome (CRS).[28] Defective organogenesis is the cause of structural damage to the fetus.[29]

CRS presents as a small-for-age infant manifesting various anomalies including cataracts (78%), sensorineural deafness (66%), and cardiac defects (58%) such as pulmonary artery stenosis, patent ductus arteriosus, and aortic coarctation.[28],[31]

Other ocular manifestations such as microphthalmia, corneal opacity, and glaucoma may be present. Findings such as blueberry muffin rash, hepatosplenomegaly, and thrombocytopenia, which are observed in other perinatal infections, can also be seen.[28] Pink pinpoint petechiae (Forchheimer spots) may be seen on the soft palate or uvula.[30]


The highest risk of CMV transmission to the fetus occurs subsequent to the primary infection of the mother, which is around 32%.[29] Maternal infection early in pregnancy is less likely to be transmitted to the fetus (around 20%), but the fetus is more likely to be symptomatic at birth and to have disabilities than with infection later in gestation. With maternal infection in the third trimester, the transmission rate is approximately 75%, but manifestation is uncommon and less severe.[32] Unlike toxoplasmosis or congenital rubella, congenital infection with CMV can also be a result of re-infection of the mother (with a different strain) or reactivation of the infection.[29]

Only 10%–15% of the neonates show features of congenital infection at birth. Around 13.5% of the rest asymptomatic newborns are at risk of developing long-term neurological sequelae, predominantly SNHL. Various manifestations of congenital infection are low birth weight, hepatic involvement, CNS involvement, and ocular or auditory damage (SNHL).[29] Cutaneous features include showers of petechiae and purpura. Presence of blueberry muffin spots indicates extramedullary hematopoiesis in congenital CMV.[29],[30]

Herpes simplex virus

Neonatal infection more commonly results from perinatal transmission than vertical transmission. Infection for the first time with HSV occurring in the mother, termed true primary infection, has the maximum risk (about 50%) for transmission. The high viral load and prolonged interval of shedding of virus in the mother may be the reasons for such high transmission. However, a decreased risk (around 30%) is observed when mothers acquire new but non-primary (infection with a different HSV type or strain) infection, and the risk is lowest (2%) when there is reactivation of maternal latent infection.[29]

Newborns infected with HSV can manifest localized disease, CNS disease, or disseminated disease, and the symptoms are exhibited by almost all the affected babies. Infection limited to the skin, eye, or oral cavity is termed as localized congenital HSV.[29] The clinical features are evident within 48 h as widespread vesiculobullous lesions, erosions, and scars. Distribution of lesions is determined by fetal presentation during birth; initial vesicles appear on the face and scalp in cephalic presentation and on the buttocks when there is breech presentation.[30] Encephalitis is a presentation of CNS disease and in case of disseminated disease, multiple organs are involved.[28]

Parvovirus B19

Congenital infection occurs when the virus is transmitted transplacentally, about 1–3 weeks (time of peak maternal viral load) following maternal infection. The maximum risk of complications to the fetus is observed when maternal infection occurs prior to the ending of the first trimester. Infection results in the characteristic slapped-cheek appearance in the baby.[28]

Fetal infection may end in spontaneous resolution or lead to consequences such as severe anemia (which in turn causes high-output cardiac failure), thrombocytopenia, nonimmune hydrops fetalis (as a result of fetal cardiac failure), maternal mirror syndrome, fetal demise, and rarely meningoencephalitis. Premature termination of pregnancy may be required owing to these complications.[28]

Perinatal infection with parvovirus causing red cell aplasia, results in persistent viremia with anemia in the infants.[28]

Human immunodeficiency virus

Various factors affecting the risk of perinatal HIV transmission are maternal plasma viral load, more advanced WHO clinical disease stage, maternal CD4 count (as the CD4 count decreases, the rate of transmission increases),[33] breastfeeding and mastitis, and acute maternal infection. Usually, the clinical manifestations of HIV infection are not seen at birth.[28]

Hepatitis B

Perinatal transmission due to exposure to blood during delivery is the most common mode of mother-to-child transmission of hepatitis B virus. Transmission occurring in utero contributes to <2% to 4%.[28] In utero transmission occurs via placenta or inhalation/chronic ingestion of the infected amniotic fluid.[28]

The highest risk of transmission of virus is seen in mothers who are acutely infected during the third trimester of gestation and in those who are HBsAg and HBeAg positive.[28]

The age of the offspring during the time of acute infection primarily determines the risk of progression to chronic hepatitis B (CHB). The occurrence of CHB is seen in about 90% of infants who are infected during delivery or in the 1st year of life.[28]

Those babies who are infected usually do not show manifestations of infection at birth or in the neonatal period.[26] Clinical hepatitis presenting as jaundice, poor feeding, and vomiting develops within few months of age.[29] In the affected infant, serum HBsAg is positive at 1–2 months of age.[28]

Hepatitis C

Hepatitis C virus (HCV) released into fetal or infant circulation as a result of exposure to mother's peripheral blood mononuclear cells infected with HCV during prenatal or perinatal period is the hypothetical mechanism of transmission postulated. However, the mode of delivery and exposure to breastmilk are not linked with the infection.[28]

Infants infected during delivery commonly do not show any symptoms. Although development of chronic HCV is seen in about 80% of infants infected perinatally, majority of them still exhibit no manifestations of infection at 5 years of age.[28]

A brief summary of the effects of various diseases on pregnancy and vice versa is shown in [Table 2].
Table 2: Effects of disease on pregnancy and vice versa

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To conclude, changes in immune function during pregnancy are responsible for the varied effects of diseases on pregnancy and the effect of pregnancy on these diseases. Therefore, a thorough knowledge regarding these effects is necessary for appropriate counseling and treatment of the anxious mother.

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Conflicts of interest

There are no conflicts of interest.

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  [Figure 1]

  [Table 1], [Table 2]


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