Many HIV-positive patients do not develop
protective antibody levels after receiving the standard dose of the swine flu
vaccine, a study published in the September 10th edition of AIDS shows. A low current CD4 cell count
was the only factor associated with a poor response to the vaccine.
“The implications of this research are
immediate for next year’s influenza vaccination campaign”, comment the investigators.
“Our results suggest that if that vaccine is used at the currently recommended
dose, a significant proportion of individuals will remain vulnerable to
It is recommended that all HIV-positive
patients should receive the seasonal flu vaccine. In 2009 the H1N1 (swine flu)
virus was identified and the World Health Organization declared a global flu
pandemic. A vaccine against the virus was developed and people with underlying
health conditions – including HIV - were recommended to receive this.
The vaccine is provided via a single
intramuscular injection, the standard dose being 15 µg. The production of an
antibody titre of at least 1: 40 on the hemagglutination-inhibition (HAI) assay
is considered protective against the virus.
Investigators from the University of
Pennsylvania wished to see if the vaccine produced protective antibody levels
in HIV-positive patients. The safety of the vaccine was also monitored.
Their study sample included 120 patients
who received the vaccine in November and December 2009. Most (71%) were men,
68% were African American, and their median age was 46.
All but one of the patients was taking
antiretroviral therapy, and the current median CD4 cell count was 502 cells/mm3.
The median nadir CD4 cell count was 132 cells/mm3. The majority
(92%) had a viral load below 400 copies/ml.
Monitoring at the time of vaccination
showed that a quarter of patients had already been exposed to swine flu and had
protective antibodies against the infection.
However, of the 90 patients without
pre-exposure to the virus, only 61% had protective levels of antibodies three
weeks after receipt of the vaccination.
Non-responders had low current (394 vs 497
cells/mm3) and nadir (112 vs 153 cells/mm3) CD4 cell
counts and had had an undetectable viral load for a shorter period of time (19
vs. 28 months) than responders.
Statistical analysis showed that the only
factor significantly associated with a poor response to the vaccine was a lower
current CD4 cell count (p = 0.019).
The vaccine was safe, the most common
side-effect being a localised, injection site reaction. This developed in 18%
“Up to 40% of HIV-positive individuals are
not seroprotected after vaccination”, write the investigators.
“The presence of other underlying chronic
diseases, medication use, poor nutrition, irreversible damage to the immune
system and immunosenescence [decline of the immune system due to ageing],
likely all play a role in decreased vaccine responsiveness in spite of successful
treatment of the HIV infection”, they add.
A number of strategies are suggested by the
researchers to enhance the response rate to the vaccination. These include the
use of alternative vaccines; increasing the dose; the use of adjuvants; and the
use of live vaccines.
The authors of an accompanying editorial
note the findings of the study, emphasising “suboptimal vaccine efficacy in
HIV-infected persons represents a clinically important matter. Current evidence
evaluating influenza vaccination efficacy in the HIV population remains