Virological suppression also corresponds with improved vaccine responsiveness, but whether this is independent
of CD4 cell count recovery is unclear [9]. In clinical practice, paediatricians commonly recommence vaccination 6 months after CD4 recovery to the normal range for age; this accords with data from a study in which children receiving primary hepatitis A virus vaccination developed greater immunity if they had been on HAART for a minimum of 6 months, compared with those on HAART for 2 months [32], but data are lacking for other vaccines. SD-208 As HAART has transformed vertically acquired HIV infection into a chronic treatable disease, attention also focuses on the durability of vaccine-induced immunity. Loss of protective immunity occurs, the extent varying with vaccine antigen. In a longitudinal study, specific antibody responses against measles, mumps and rubella were lost in 40, 38 and 11%, respectively, SGI-1776 of 59 children who were seropositive at baseline, despite apparent immune reconstitution on HAART [33]. Older children and adolescents may have been adequately immunized in the first years of life but can lose specific antibodies despite effective HAART,
becoming susceptible to infections such as pneumococcus and pertussis [34]. Despite good initial responses to primary immunization, a single reinforcing dose may be insufficient to sustain long-term protection; additional booster doses of vaccines or complete revaccination may be required to restore sustained protection Cyclooxygenase (COX) in older children. While it is postulated that detectable HIV viraemia may be detrimental to vaccine responsiveness in children and adolescents [9], data are very limited for infants receiving primary vaccination. Consensus is lacking in this regard: some clinicians empirically advocate postponing primary immunizations in the short term until viraemia is controlled, in order to optimize the potential for protective responses; others advocate vaccination on schedule on the grounds that immune function is usually preserved in infancy,
that deferring vaccinations increases infants’ risk of vaccine-preventable diseases, and that departure from the schedule risks reducing vaccine coverage. Specific studies are required to resolve this and to determine the benefits of additional strategies for protecting infants such as vaccinating household contacts. The emerging picture is that HIV-positive children vaccinated in accordance with routine schedules, even those with numerically acceptable immune status, on or off HAART, are likely to have suboptimal and short-lived immunity to certain vaccines, and this may not be reversed or fully prevented by HAART unless started very early in life. The pace of immune recovery on HAART differs between pathogens [35, 36], so it is unsurprising that the same holds true for different vaccines.
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