Skip Navigation LinksHome > September 10, 2010 - Volume 24 - Issue 14 > Poor immunogenicity of the H1N1 2009 vaccine in well control...
AIDS:
doi: 10.1097/QAD.0b013e32833c6d5c
Clinical Science

Poor immunogenicity of the H1N1 2009 vaccine in well controlled HIV-infected individuals

Tebas, Pabloa; Frank, Iana; Lewis, Markb; Quinn, Josepha; Zifchak, Larisaa; Thomas, Aleshiaa; Kenney, Thomasa; Kappes, Rosemarya; Wagner, Waynea; Maffei, Kathya; Sullivan, Kathleena; the Center for AIDS Research and Clinical Trials Unit of the University of Pennsylvania

Free Access
Article Outline
Collapse Box

Author Information

aAIDS Clinical Trials Unit, University of Pennsylvania School of Medicine, Philadelphia, Pennsylvania, USA

bBIOQUAL Inc., Rockville, Maryland, USA.

Received 16 March, 2010

Revised 3 May, 2010

Accepted 24 May, 2010

Correspondence to Pablo Tebas, MD, AIDS Clinical Trials Unit, University of Pennsylvania, Philadelphia, Pennsylvania, USA. E-mail: pablo.tebas@uphs.upenn.edu

Collapse Box

Abstract

Objective: To evaluate the safety and immunogenicity of the H1N1 2009 vaccine in HIV-positive individuals.

Design: A single-arm study.

Setting: Clinic at the Hospital of the University of Pennsylvania, Philadelphia, Pennsylvania, USA.

Participants: HIV-infected adults with an indication for H1N1 vaccination.

Intervention: Single intramuscular 15 μg dose of the monovalent, unadjuvanted, inactivated, split virus H1N1 vaccine.

Main outcomes: Immunogenicity, safety and tolerability.

Results: A total of 120 participants were enrolled, 71% men, 68% African–American, with median age of 46 years. All of them but one were on antiretroviral treatment, with a median current CD4 cell counts of 502 cells/μl, and a nadir CD4 cell counts of 132 cells/μl. The HIV RNA level was below 400 copies/ml in 92% of participants. All participants completed the 3 weeks of follow-up. Thirty of the 120 (25%) participants had antibody hemagglutination-inhibition assay titers equal or greater than 1: 40 at baseline. Among participants without evidence of previous exposure, only 61% develop protective titers by week 3 of the study. Nonresponders had lower current and nadir CD4 cell counts than responders. Only four of nine participants with detectable HIV viral load at baseline developed protective antibody titers. Age and race were not predictors of the response to the vaccine. The vaccine was well tolerated.

Conclusion: These results suggest that only 60% of well controlled HIV-infected individuals without preexisting immunity to H1N1 develop protective antibody titers after immunization. Alternative vaccines, dosing, adjuvants or schedule strategies are needed to achieve effective immunization of this vulnerable population.

Back to Top | Article Outline

Introduction

The emergence of a new distinct subtype of the influenza virus has the potential to produce global pandemics that can lead to significant morbidity and mortality if the new strain is particularly pathogenic. During the spring of 2009, a novel influenza A H1N1 virus was identified, initially in Mexico and the USA and spreading quickly to the rest of the world. In June 2009, the WHO declared a flu pandemic, only the fourth of the last century [1].

Some immunosuppressed individuals are at an increased risk of developing complications after influenza infections [2]. Although there are scant data supporting that patients with HIV infection have a higher influenza case rate [3,4], several studies have demonstrated that HIV-infected patients are more likely to have severe or prolonged influenza infections [5,6]. The widespread use of HAART has decreased the rate of complications of influenza in HIV-infected individuals, but has not brought them down to the rate of the uninfected population [7]. As a consequence of this, treatment guidelines recommend yearly influenza vaccination for all patients with HIV infection [8,9]. The transient increases in HIV replication observed after influenza vaccination has not translated into long-term deleterious effects [10–15]. Multiple studies have demonstrated that antibody responses after influenza immunization among HIV-infected individuals are poorer than in the general population, although this finding has not been consistent across all studies [16–23]. The main predictors of vaccine responses in this population have been the CD4 cell counts [24] and the presence of HIV viremia [23,25]. Except for a few studies [24,26], almost all trials evaluating immunological responses to the influenza vaccine among HIV-positive individuals have looked at serological responses rather than the incidence of clinical influenza [27].

Several epidemiologic studies describing risk factors for severe H1N1 infection do not separate HIV infection from other immunosuppressive states, they have shown consistently that individuals with underlying immunosuppression are more prone to both infection and more severe cases of influenza [28,29]. This has been particularly worrisome in South Africa, where 53% of the deaths from H1N1 had underlying HIV infection [30], raising concerns of the potential lethality of this infection in these patients, particularly in the developing world. Mexico's data suggest that patients with CD4 cell counts less than 200 cells/μl or an opportunistic infection are at particular risk for complications requiring inpatient care [relative risk (RR) 24.5] and mechanical ventilation (RR 19.7) [31]. However, in the developed world, the rate of infection and complications after H1N1 infection is similar or lower in HIV-infected individuals when compared with HIV-negative individuals [32,33].

We conducted this study to evaluate the immunogenicity, safety and tolerability of one of the currently approved and recommended H1N1 vaccinations for HIV-infected individuals.

Back to Top | Article Outline

Methods

Vaccine

We evaluated the immunogenicity, safety and tolerability of the recommended single intramuscular 15 μg dose of the monovalent, unadjuvanted, inactivated, split virus H1N1 vaccine (Novartis, Basel, Switzerland). Each participant had baseline studies performed at the time of enrollment followed by the intramuscular administration in one of the deltoid muscles of the 2009 H1N1 influenza vaccine (0.5 ml), followed by two phone calls and serological response evaluations completed 21–28 days after vaccination. Our hypothesis was that the response to the new H1N1 vaccine would be compromised in patients with HIV infection.

Back to Top | Article Outline
Participants

We included HIV-infected individuals, older than 18 years of age, who had an indication to receive the H1N1 vaccine. We excluded individuals with a known allergy to eggs or other components of the vaccine, a history of severe reactions to previous immunization with seasonal flu, known cases of H1N1 influenza during the spring of 2009 or previous recipients of the novel H1N1 vaccine. We also excluded recipients of other licensed live vaccines within 4 weeks or inactivated vaccines within 1 week of study entry. Patients receiving experimental treatments (except participants of phase III antiretroviral trials), systemic chemotherapy for the previous 36 months, steroids and other immunomodulators, or with a history of Guillain–Barré syndrome were also excluded.

Sequential clinic patients who agreed to participate were enrolled. The study was conducted at the MacGregor Clinic of the Hospital of the University of Pennsylvania in Philadelphia, Pennsylvania, USA, between the months of November and January 2009–2010. All patients signed an informed consent. The study was approved by the University of Pennsylvania institutional review board and registered in clinical trials.gov #NCT01111162.

Back to Top | Article Outline
Endpoints

The primary immunogenicity endpoint of the study was the proportion of participants with antibody titers equal or greater than 1: 40 on the hemagglutination-inhibition (HAI) assay. The primary safety endpoint was the frequency, duration and intensity of adverse events after vaccination [solicited, local and systemic, using the HIV Vaccine Trials Network (HVTN) questionnaire]. Seroconversion was defined as a four-fold increase from baseline titers.

Back to Top | Article Outline
Safety assessments

We collected local and systemic adverse events using a modified HIV Vaccine Trials Network (HVTN) questionnaire, which has been validated by the HVTN. We used the standard AIDS Clinical Trials Group grading scale to evaluate adverse events.

Back to Top | Article Outline
Immunological assessments

We measured anti-HAI assay antibody titers at baseline and at week 3 (+7 days) after immunization, using the HAI assay against the H1N1 (A/California/04/2009) strain (Bioqual, Inc., Rockville, Maryland, USA).

Back to Top | Article Outline
Hemagglutination inhibition assay

Sera were treated with receptor-destroying enzyme (RDE) by diluting one part serum with three parts enzyme and incubated overnight at 37°C in a water bath. The enzyme was inactivated by 30-min incubation at 56°C followed by adsorption to red blood cells (RBCs) and addition of phosphate buffer saline for a final dilution of 1/10. HAI assays were performed in V-bottom 96-well plates using four hemagglutinating units (HAU) of virus and 0.5% turkey RBCs.

Back to Top | Article Outline
Statistical analysis

A total of 120 participants were enrolled. We anticipated that up to 20% of the participants would not come for the second blood draw at 21–28 days. Finding of no grade 3 or grade 4 adverse events in a total evaluable sample of 100 participants would provide 95% confidence that the rate in the population from which the sample was drawn is no greater than 3%. Finding of 75 immunological responders in the total sample of 100 participants would provide 95% confidence that the rate of response in the population from which the sample was drawn was no lower than 67% (PASS 2008; NCSS, LLC., Kaysville, Utah, USA). Summary statistics for continuous variables are presented as median (first quartile–third quartile). Comparison between treatment arms was carried out using a Mann–Whitney U test for continuous variables, and a Fisher's exact test or Pearson's χ2 test for categorical factors. A logistic regression model was constructed to evaluate current and nadir CD4 cell counts, viral load (undetectable or not), age and race as predictors of response or not to the H1N1 vaccine. The SPSS statistical package (version 17.0; SPSS, Inc., Chicago, Illinois, USA) was used for the analysis of the trial data.

Back to Top | Article Outline

Results

From 20 November to 17 December 2009, we enrolled 120 participants. All vaccinated participants completed the second visit at 21–28 days after immunization. All 120 participants are included in the immunogenicity and safety analysis.

The participants' baseline characteristics are summarized in Table 1. Participants were mostly men (85%) and African–American (68%). All but one were receiving antiretroviral therapy (ART), and most of them had an HIV RNA viral load below 400 copies/ml (92%, 84% of them below the limit of quantification using the ultrasensitive assay) for a median of 26 months. The median nadir CD4 cells count of patients was 131 cells/μl, and the current CD4 cells count was 502 cells/μl.

Table 1
Table 1
Image Tools

Thirty of the 120 (25%) participants had antibody HAI assay titers equal or greater than 1: 40 at baseline. At week 3, 69% of participants achieved antibody levels equal or above 1: 40 (Fig. 1). Among the 90 participants without evidence of previous exposure to H1N1, only 61% [95% confidence interval (CI) 51–71] developed protective titers by week 3 of the study. Nonresponders had lower current (394 vs. 497 cells/μl) and nadir CD4 cell counts (112 vs. 153 cells/μl) and had an undetectable HIV viral load for a shorter period of time than responders (19 vs. 28 months), although those differences did not reach statistical significance (Table 2). Only four out of nine participants with detectable HIV viral load at baseline (and no evidence of prior infection) developed protective antibody titers. Race and age did not differ among responders and nonresponders to the vaccine. The rate of seroconversion (a four-fold increase from baseline titers) was 56% (95% CI 47–65). Among participants with baseline titers below 1: 40, the rate of seroconversion was 53% (95% CI 34–72), and for those with baseline titers greater than or equal 1: 40, it was 57% (95% CI 46–67) (P = NS).

Fig. 1
Fig. 1
Image Tools
Table 2
Table 2
Image Tools

In a logistic regression model that evaluated current and nadir CD4 cell counts, viral load, sex, age and race as potential predictors, only current CD4 cells count (P = 0.019) was associated independently with a vaccine response. Among participants in the lowest quartile of current CD4 cell counts (31–306 cells/μl), only 43% had seroprotection at the end of the study compared with approximately 60% among participants in the three highest quartiles (Fig. 2).

Fig. 2
Fig. 2
Image Tools

The vaccine was well tolerated with grade 1 local reactions at the site of injection, observed in 18% of the participants. There were no serious adverse events. Figure 3 summarizes adverse events observed. The most frequent local adverse events were pain and tenderness at the injection site. The most frequent systemic side effect was malaise followed by headache and myalgias.

Fig. 3
Fig. 3
Image Tools
Back to Top | Article Outline

Discussion

H1N1 vaccination has been clearly effective in the adult healthy population. A single 15 μg dose of 2009 H1N1 vaccine was immunogenic in adults, with mild-to-moderate vaccine-associated reactions. More than 95% of the recipients developed protective antibody titers [34].

Our study shows that independently of virological control and CD4 recovery, up to 40% of HIV-positive individuals are not seroprotected after vaccination. The presence of other underlying chronic diseases, medication use, poor nutrition, irreversible damage to the immune system and immunosenescence, likely all play a role in decreased vaccine responsiveness in spite of the successful treatment of the HIV infection.

The implications of this research are immediate for next year's influenza vaccination campaign, which will substitute the H1N1 component of the trivalent vaccine (the only one currently approved for use in HIV-infected individuals) with the 2009 H1N1 pandemic strain. Our results suggest that if that vaccine is used at the currently recommended dose, a significant proportion of the individuals will remain vulnerable to influenza. Furthermore, although some studies suggest otherwise [24], a 1: 40 titer may not be fully protective in immune-compromised individuals.

What strategies can be used to improve these immunological responses? Higher dose of the antigen has been associated with higher antibody titers in many studies and can improve the immunogenicity of the influenza vaccine in poorly responsive populations such as the elderly [35]. This strategy in adult HIV-infected individuals is currently being evaluated in two National Institutes of Health sponsored studies (clinical trials.gov #NCT00996970 and #NCT00992433). Another strategy to improve immunogenicity in the population of HIV-infected individuals is the use of adjuvants that can increase the responsiveness to this and other vaccines [36]. During the 2010 Conference of Retrovirus and Opportunistic infections in San Francisco, two studies using the same AS03A-adjuvanted H1N1v vaccine showed divergent results, one positive [37] and one negative [38]; however, the use of adjuvanted influenza vaccines have not been approved in the United States. The use of the live virus vaccine may improve responses, but recent studies in adults suggest that this vaccine is less immunogenic in adults than the trivalent vaccine, particularly in those individuals with some degree of preexisting immunity [39], and this live attenuated vaccine is not approved for use in HIV-infected individuals in spite of some promising preliminary results [40,41].

In our study, current CD4 cells count, and not nadir CD4 cells count, was the strongest predictor of vaccine response. We had a very small proportion of patients with detectable viremia and, therefore, our study was underpowered to evaluate the effects of persistent viremia in vaccine responsiveness, which in other studies have been associated with vaccine's responsiveness [42]. Thanks to the advances on ART, the population of patients with detectable viremia in HIV-infected patients in care is dwindling; however, they probably constitute a population with high risk for poor responses to vaccination and another reason to the growing number of arguments to consider earlier treatment of HIV infection.

Because of the advances of antiretroviral treatment and the increased survival of patients with HIV infection, the prevalence of HIV infection in the population will continue to grow both in the developed and the developing world. Alternative vaccines, dosing, adjuvants or schedule strategies are needed to achieve effective immunization of this vulnerable population. The 2009 H1N1 infection, though less severe than originally feared, could serve as a good model for future, potentially more deadly pandemics. Lessons learned from this epidemic can, and should, be applied in the future and help in the design and development of more effective vaccines.

Back to Top | Article Outline

Acknowledgements

The study was supported in part by the National Institute of Allergy and Infectious Diseases grant #U01-AI069467 and the Center for AIDS Research grant #P30-AI045008 to the University of Pennsylvania.

All authors participated in the design, implementation, analysis and interpretation of the study.

There are no conflicts of interest.

Back to Top | Article Outline

References

1. WHO. Pandemic (H1N1) 2009. Geneva, Switzerland: WHO; 2010.

2. Kunisaki KM, Janoff EN. Influenza in immunosuppressed populations: a review of infection frequency, morbidity, mortality, and vaccine responses. Lancet Infect Dis 2009; 9:493–504.

3. Cohen JP, Macauley C. Susceptibility to influenza A in HIV-positive patients. JAMA 1989; 261:245.

4. Fine AD, Bridges CB, De Guzman AM, Glover L, Zeller B, Wong SJ, et al. Influenza a among patients with human immunodeficiency virus: an outbreak of infection at a residential facility in New York City. Clin Infect Dis 2001; 32:1784–1791.

5. Neuzil KM, Reed GW, Mitchel EF Jr, Griffin MR. Influenza-associated morbidity and mortality in young and middle-aged women. JAMA 1999; 281:901–907.

6. Lin JC, Nichol KL. Excess mortality due to pneumonia or influenza during influenza seasons among persons with acquired immunodeficiency syndrome. Arch Intern Med 2001; 161:441–446.

7. Neuzil KM, Coffey CS, Mitchel EF Jr, Griffin MR. Cardiopulmonary hospitalizations during influenza season in adults and adolescents with advanced HIV infection. J Acquir Immune Defic Syndr 2003; 34:304–307.

8. Aberg JA, Gallant JE, Anderson J, Oleske JM, Libman H, Currier JS, et al. Primary care guidelines for the management of persons infected with human immunodeficiency virus: recommendations of the HIV Medicine Association of the Infectious Diseases Society of America. Clin Infect Dis 2004; 39:609–629.

9. Fiore AE, Shay DK, Haber P, Iskander JK, Uyeki TM, Mootrey G, et al. Prevention and control of influenza. Recommendations of the Advisory Committee on Immunization Practices (ACIP), 2007. MMWR Morb Mortal Wkly Rep 2007; 56:1–54.

10. Staprans SI, Hamilton BL, Follansbee SE, Elbeik T, Barbosa P, Grant RM, et al. Activation of virus replication after vaccination of HIV-1-infected individuals. J Exp Med 1995; 182:1727–1737.

11. Røsok B, Voltersvik P, Bjerknes R, Axelsson M, Haaheim LR, Åsjö B. Dynamics of HIV-1 replication following influenza vaccination of HIV+ individuals. Clin Exp Immunol 1996; 104:203–207.

12. Tasker SA, O'Brien WA, Treanor JJ, Weiss PJ, Olson PE, Kaplan AH, et al. Effects of influenza vaccination in HIV-infected adults: a double-blind, placebo-controlled trial. Vaccine 1998; 16:1039–1042.

13. Günthard HF, Wong JK, Spina CA, Ignacio C, Kwok S, Christopherson C, et al. Effect of influenza vaccination on viral replication and immune response in persons infected with human immunodeficiency virus receiving potent antiretroviral therapy. J Infect Dis 2000; 181:522–531.

14. Kolber MA, Gabr AH, De la Rosa A, Glock JA, Jayaweera D, Miller N, et al. Genotypic analysis of plasma HIV-1 RNA after influenza vaccination of patients with previously undetectable viral loads. AIDS 2002; 16:537–542.

15. Glesby MJ, Hoover DR, Farzadegan H, Margolick JB, Saah AJ. The effect of influenza vaccination on human immunodeficiency virus type 1 load: A randomized, double-blind, placebo-controlled study. J Infect Dis 1996; 174:1332–1336.

16. Ragni MV, Ruben FL, Winkelstein A. Antibody responses to immunization of patients with hemophilia with and without evidence of human immunodeficiency virus (human T-lymphotropic virus type III) infection. J Lab Clin Med 1987; 109:545–549.

17. Nelson KE, Clements ML, Miotti P, Cohn S, Polk BF. The influence of human immunodeficiency virus (HIV) infection on antibody responses to influenza vaccines. Ann Intern Med 1988; 109:383–388.

18. Miotti PG, Nelson KE, Dallabetta GA, Farzadegan H, Margolick J, Clements ML. The influence of HIV infection on antibody responses to a two-dose regimen of influenza vaccine. JAMA 1989; 262:779–783.

19. Kroon FP, Rimmelzwaan GF, Roos MTL, Osterhaus ADME, Hamann D, Miedema F, et al. Restored humoral immune response to influenza vaccination in HIV-infected adults treated with highly active antiretroviral therapy. AIDS 1998; 12:F217–F223.

20. Brydak LB, Hryniewicz HJ, Machala M, Horban A. Humoral response to influenza vaccination in HIV-infected patients. Clin Drug Investig 1999; 17:441–449.

21. Zanetti AR, Amendola A, Besana S, Boschini A, Tanzi E. Safety and immunogenicity of influenza vaccination in individuals infected with HIV. Vaccine 2002; 20 (Suppl 5):B29–B32.

22. Durando P, Fenoglio D, Boschini A, Ansaldi F, Icardi G, Sticchi L, et al. Safety and immunogenicity of two influenza virus subunit vaccines, with or without MF59 adjuvant, administered to human immunodeficiency virus type 1-seropositive and -seronegative adults. Clin Vaccine Immunol 2008; 15:253–259.

23. Evison J, Farese S, Seitz M, Uehlinger DE, Furrer H, Muhlemann K. Randomized, double-blind comparative trial of subunit and virosomal influenza vaccines for immunocompromised patients. Clin Infect Dis 2009; 48:1402–1412.

24. Yamanaka H, Teruya K, Tanaka M, Kikuchi Y, Takahashi T, Kimura S, et al. Efficacy and immunologic responses to influenza vaccine in HIV-1-infected patients. J Acquir Immune Defic Syndr 2005; 39:167–173.

25. Fuller JD, Craven DE, Steger KA, Cox N, Heeren TC, Chernoff D. Influenza vaccination of human immunodeficiency virus (HIV)-infected adults: impact on plasma levels of HIV type 1 RNA and determinants of antibody response. Clin Infect Dis 1999; 28:541–547.

26. Tasker SA, Treanor JJ, Paxton WB, Wallace MR. Efficacy of influenza vaccination in HIV-infected persons: a randomized, double-blind, placebo-controlled trial. Ann Intern Med 1999; 131:430–433.

27. Anema A, Mills E, Montaner J, Brownstein JS, Cooper C. Efficacy of influenza vaccination in HIV-positive patients: a systematic review and meta-analysis. HIV Med 2008; 9:57–61.

28. Gilsdorf A, Poggensee G. Influenza A (H1N1)v in Germany: the first 10,000 cases. Euro Surveill 2009; 14:pii, 19318.

29. Oliveira W, Carmo E, Penna G, Kuchenbecker R, Santos H, Araujo W, et al. Pandemic H1N1 influenza in Brazil: analysis of the first 34,506 notified cases of influenza-like illness with severe acute respiratory infection (SARI). Euro Surveill 2009; 14:pii, 19362.

30. Archer B, Cohen C, Naidoo D, Thomas J, Makunga C, Blumberg L, et al. Interim report on pandemic H1N1 influenza virus infections in South Africa, April to October 2009: epidemiology and factors associated with fatal cases. Euro Surveill 2009; 14:pii, 19369.

31. Reyes-Terán G, Rosa-Zamboni D, Ormsby C, Vazquez-Perez J, Ablanedo-Terrazas Y, Vega-Barrientos R, et al. Clinical features of subjects infected with HIV and H1N1 influenza virus [abstract #803LB]. In: Conference on Retrovirus and Opportunistic Infections; 16–19 February 2010; San Francisco, California, USA; 2010.

32. Keri Althoff K, Gange S, Sharp G, Eichelberger M, Gao J, Glesby M, et al. Elevated 2009 H1N1 antibody titers in HIV-infected and uninfected women in the US: a Sero-study, March 1 to September 30, 2009 [abstract #807LB]. In: Conference on Retrovirus and Opportunistic Infections; 16–19 February 2010; San Francisco, California, USA; 2010.

33. Martinez E, Maros M, Hoyo I, Anton A, Sanchez M, Vilella A, et al. 2009 H1N1 virus infection in HIV+ adults [abstract #802LB]. In: Conference on Retrovirus and Opportunistic Infections; 16–19 February 2010; San Francisco, California, USA; 2010.

34. Greenberg ME, Lai MH, Hartel GF, Wichems CH, Gittleson C, Bennet J, et al. Response to a monovalent 2009 influenza A (H1N1) Vaccine. N Engl J Med 2009; 361:2405–2413.

35. Falsey AR, Treanor JJ, Tornieporth N, Capellan J, Gorse GJ. Randomized, double-blind controlled phase 3 trial comparing the immunogenicity of high-dose and standard-dose influenza vaccine in adults 65 years of age and older. J Infect Dis 2009; 200:172–180.

36. Leroux-Roels I, Borkowski A, Vanwolleghem T, Drame M, Clement F, Hons E, et al. Antigen sparing and cross-reactive immunity with an adjuvanted rH5N1 prototype pandemic influenza vaccine: a randomised controlled trial. Lancet 2007; 370:580–589.

37. Launay O, Desaint C, Durier C, Loulergue P, Duval X, Pialoux G, et al. Immunogenicity of one dose of influenza A H1N1v 2009 vaccine formulated with and without AS03A-adjuvant in HIV+ adults: preliminary report of the ANRS 151 randomized HIFLUVAC trial [abstract #804LB]. In: Conference on Retrovirus and Opportunistic Infections; 16–19 February 2010; San Francisco, California, USA; 2010.

38. Bickel M, Wieters I, von Hentig N, Khaykin P, Nisius G, Haberl A, et al. Low rate of immunoresponse to the novel split virion, inactivated, adjuvanted pandemic H1N1 influenza vaccine in HIV-1-infected patients [abstract #805LB]. In: Conference on Retrovirus and Opportunistic Infections; 16–19 February 2010; San Francisco, California, USA; 2010.

39. Monto AS, Ohmit SE, Petrie JG, Johnson E, Truscon R, Teich E, et al. Comparative efficacy of inactivated and live attenuated influenza vaccines. N Engl J Med 2009; 361:1260–1267.

40. King JC, Treanor J, Fast PE, Wolff M, Yan LH, Iacuzio D, et al. Comparison of the safety, vaccine virus shedding, and immunogenicity of influenza virus vaccine, trivalent, types A and B, live cold-adapted, administered to human immunodeficiency virus (HIV)-infected and non-HIV-infected adults. J Infect Dis 2000; 181:725–728.

41. Levin MJ, Song L-Y, Fenton T, Nachman S, Patterson J, Walker R, et al. Shedding of live vaccine virus, comparative safety, and influenza-specific antibody responses after administration of live attenuated and inactivated trivalent influenza vaccines to HIV-infected children. Vaccine 2008; 26:4210–4217.

42. Overton ET, Sungkanuparph S, Powderly WG, Seyfried W, Groger RK, Aberg JA. Undetectable plasma HIV RNA load predicts success after hepatitis B vaccination in HIV-infected persons. Clin Infect Dis 2005; 41:1045–1048.

Cited By:

This article has been cited 13 time(s).

Annals of Internal Medicine
Improved Immunogenicity With High-Dose Seasonal Influenza Vaccine in HIV-Infected Persons A Single-Center, Parallel, Randomized Trial
McKittrick, N; Frank, I; Jacobson, JM; White, CJ; Kim, D; Kappes, R; DiGiorgio, C; Kenney, T; Boyer, J; Tebas, P
Annals of Internal Medicine, 158(1): 19-U62.

Human Vaccines & Immunotherapeutics
Immune reconstitution and vaccination outcome in HIV-1 infected children Present knowledge and future directions
Cagigi, A; Cotugno, N; Giaquinto, C; Nicolosi, L; Bernardi, S; Rossi, P; Douagi, I; Palma, P
Human Vaccines & Immunotherapeutics, 8(): 1784-1794.
10.4161/hv.21827
CrossRef
Human Vaccines & Immunotherapeutics
Immune response to 2009 H1N1 vaccine in HIV-infected adults in Northern Thailand
Chotirosniramit, N; Sugandhavesa, P; Aurpibul, L; Thetket, S; Kosashunhanan, N; Supindham, T; Wongkulab, P; Kaewpoowat, Q; Chaiklang, K; Kaewthip, O; Sroysuwan, P; Wongthanee, A; Lerdsamran, H; Puthavathana, P; Suparatpinyo, K
Human Vaccines & Immunotherapeutics, 8(): 1854-1859.
10.4161/hv.21820
CrossRef
Vaccine
Relation of activation-induced deaminase (AID) expression with antibody response to A(H1N1)pdm09 vaccination in HIV-1 infected patients
Cagigi, A; Pensieroso, S; Ruffin, N; Sammicheli, S; Thorstensson, R; Pan-Hammarstrom, Q; Hejdeman, B; Nilsson, A; Chiodi, F
Vaccine, 31(): 2231-2237.
10.1016/j.vaccine.2013.03.002
CrossRef
Hiv Clinical Trials
Immune Response after a Single Dose of the 2010/11 Trivalent, Seasonal Influenza Vaccine in HIV-1-Infected Patients and Healthy Controls
Bickel, M; Lassmann, C; Wieters, I; Doerr, HW; Herrmann, E; Wicker, S; Brodt, HR; Stephan, C; Allwinn, R; Jung, O
Hiv Clinical Trials, 14(4): 175-181.
10.1310/hct1404-175
CrossRef
AIDS Reviews
Vaccinating HIV Patients: Focus on Human Papillomavirus and Herpes Zoster Vaccines
Koenig, HC; Garland, JM; Weissman, D; Mounzer, K
AIDS Reviews, 15(2): 77-86.

Disease Markers
Immune Activation and Viral Replication after Vaccination with an Influenza A H1N1 2009 Vaccine in HIV-Infected Children Receiving Antiretroviral Therapy
Onlamoon, N; Unpol, P; Boonchan, M; Sukapirom, K; Wittawatmongkol, O; Chokephaibulkit, K; Ammaranond, P; Pattanapanyasat, K
Disease Markers, (): -.
10.1155/2013/276547
CrossRef
AIDS Research and Human Retroviruses
Cellular and Humoral Immune Responses to Pandemic Influenza Vaccine in Healthy and in Highly Active Antiretroviral Therapy-Treated HIV Patients
Agrati, C; Gioia, C; Castilletti, C; Lapa, D; Berno, G; Puro, V; Carletti, F; Cimini, E; Nisii, C; Castellino, F; Martini, F; Capobianchi, MR
AIDS Research and Human Retroviruses, 28(): 1606-1616.
10.1089/aid.2011.0371
CrossRef
Clinical Infectious Diseases
Safety and Immunogenicity of 2009 pH1N1 Vaccination in HIV-Infected Pregnant Women
Abzug, MJ; Nachman, SA; Muresan, P; Handelsman, E; Watts, DH; Fenton, T; Heckman, B; Petzold, E; Weinberg, A; Levin, MJ
Clinical Infectious Diseases, 56(): 1488-1497.
10.1093/cid/cit057
CrossRef
Vaccine
Immune response after one or two doses of pandemic influenza A (H1N1) monovalent, AS03-adjuvanted vaccine in HIV infected adults
Nielsen, AB; Nielsen, HS; Nielsen, L; Thybo, S; Kronborg, G
Vaccine, 30(): 7067-7071.
10.1016/j.vaccine.2012.09.052
CrossRef
Acta Virologica
Immunogenicity and safety of pandemic H1N1 2009 influenza vaccine for HIV-1 patients
Jilich, D; Havlickova, M; Vesely, D; Rozsypal, H; Jirincova, H; Stankova, M; Kyncl, J; Maly, M; Machala, L
Acta Virologica, 56(4): 349-351.
10.4149/av_2012_04_349
CrossRef
Clinical and Vaccine Immunology
Absolute Lymphocyte Count Predicts the Response to New Influenza Virus H1N1 Vaccination in Pediatric Cancer Patients
Mavinkurve-Groothuis, AMC; van der Flier, M; Stelma, F; van Leer-Buter, C; Preijers, FW; Hoogerbrugge, PM
Clinical and Vaccine Immunology, 20(1): 118-121.
10.1128/CVI.00585-12
CrossRef
AIDS
Preventing influenza coinfection among HIV-infected persons: a complex picture coming into focus
Reyes-Teran, G; Butera, ST
AIDS, 24(14): 2283-2285.
10.1097/QAD.0b013e32833dbcd2
PDF (94) | CrossRef
Back to Top | Article Outline
Keywords:

2009 H1N1; immunogenicity; vaccine

© 2010 Lippincott Williams & Wilkins, Inc.

Login

Search for Similar Articles
You may search for similar articles that contain these same keywords or you may modify the keyword list to augment your search.