The spread of neonatal herpes
Mothers who acquire genital herpes in the last few weeks of pregnancy are at highest risk of transmitting the virus to their babies. If maternal infection is the primary right (he has no previous antibodies to either HSV-1 or HSV-2), and he seroconverts (a positive HSV) in late pregnancy, the risk of transmission can be as high as 50%, according to research by Brown and others. The risk is too high if he had prior infection with HSV-1 but not HSV-2. While the acquisition of herpes in the last few weeks of pregnancy is very rare, may account for nearly half of all cases of neonatal herpes. If a woman has primary herpes at any point in pregnancy, there is also the possibility of the virus crossing the placenta and infect the baby in the womb. About 5% of neonatal herpes cases are contracted this way.
In about 90% of cases, neonatal herpes is transmitted when a baby comes into contact with HSV-1 or 2 in the birth canal during labor. There is a high risk of transmission if the mother has an active outbreak, because of the possibility of high viral shedding during an outbreak. There is also a small risk of transmission from asymptomatic shedding (when the virus reactivates without causing any symptoms).
Fortunately, the infants of mothers with long herpes infection have a natural protection against viruses. Herpes antibodies in the mother’s blood cross the placenta into the fetus. These antibodies help protect the baby from contracting the infection during birth, even if there is some virus in the birth canal. That’s the main reason that mothers with recurrent genital herpes rarely transmit herpes to their babies during delivery. Even women who get genital herpes during the first two trimesters of pregnancy can usually supply sufficient antibodies to help protect the fetus.
Babies born prematurely may be at slightly increased risk, however, even if the mother has a past infection. This is because the transfer of maternal antibodies to the fetus beginning around 28 weeks of gestation and continues until birth. "Babies delivered at term should be protected by the antibodies – but premature babies do not get a full load," explains Brown.
Mothers who get genital herpes during the last trimester of pregnancy may also lack the time to make enough antibodies to send through the placenta. In addition, people newly infected – whether pregnant or not – have higher rates of asymptomatic shedding for about a year after the primary episode. These higher levels of asymptomatic shedding, plus the lack of antibodies, creating a greater risk to infants whose mothers were infected during the last trimester.
Finally, around 5% -8% of the infants who contracted herpes-infected neonate after birth, often when they kissed – by adults who have active infections of oral herpes (cold sores).

