Pandemic influenza A (H1N1) in HIV-1-infected patients

Pérez, Carlos M.; Domínguez, María Isabel; Ceballos, María Elena; Moreno, Cristina; Labarca, Jaime; Rabagliati, Ricardo; Vásquez, Patricia; Lasso, Martín; Serri, Michel

doi:10.1097/qad.0b013e32833e92d5

Cited by 18 publications

(8 citation statements)

References 3 publications

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“…The retention of functions by the influenza-specific CD8 T cells during early SIV infection was somewhat surprising given the broad immunodeficiency induced by SIV. Indeed it was recently shown that some influenza strains can be more pathogenic in HIV-infected humans compared to HIV-negative humans, suggesting influenza-specific immunity is impaired during HIV infection [59]. On the other hand, in our study the SIV-specific CD8 T cells are actively responding to a persistent viral infection whereas the influenza-specific CD8 T cells are no longer responding to an antigenic challenge.…”

Section: Discussioncontrasting

confidence: 45%

Comparison of Influenza and SIV Specific CD8 T Cell Responses in Macaques

et al. 2012

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Macaques are a potentially useful non-human primate model to compare memory T-cell immunity to acute virus pathogens such as influenza virus and effector T-cell responses to chronic viral pathogens such as SIV. However, immunological reagents to study influenza CD8+ T-cell responses in the macaque model are limited. We recently developed an influenza-SIV vaccination model of pigtail macaques (Macaca nemestrina) and used this to study both influenza-specific and SIV-specific CD8+ T-cells in 39 pigtail macaques expressing the common Mane-A*10+ (Mane-A01*084) MHC-I allele. To perform comparative studies between influenza and SIV responses a common influenza nucleoprotein-specific CD8+ T-cell response was mapped to a minimal epitope (termed RA9), MHC-restricted to Mane-A*10 and an MHC tetramer developed to study this response. Influenza-specific memory CD8+ T-cell response maintained a highly functional profile in terms of multitude of effector molecule expression (CD107a, IFN-γ, TNF-α, MIP-1β and IL-2) and showed high avidity even in the setting of SIV infection. In contrast, within weeks following active SIV infection, SIV-specific CD8+ effector T-cells expressed fewer cytokines/degranulation markers and had a lower avidity compared to influenza specific CD8+ T-cells. Further, the influenza specific memory CD8 T-cell response retained stable expression of the exhaustion marker programmed death-marker-1 (PD-1) and co-stimulatory molecule CD28 following infection with SIV. This contrasted with the effector SIV-specific CD8+ T-cells following SIV infection which expressed significantly higher amounts of PD-1 and lower amounts of CD28. Our results suggest that strategies to maintain a more functional CD8+ T-cell response, profile may assist in controlling HIV disease.

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Section: Discussioncontrasting

confidence: 45%

Comparison of Influenza and SIV Specific CD8 T Cell Responses in Macaques

et al. 2012

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“…In fact, cases of severe complications with onset of pneumonia that led to hospitalization and that, in one case, required oxygen supplementation, were detected only in HIV-negative patients. This is in apparent contrast with previous findings, where no remarkable differences in clinical outcomes were observed in HIV-positive patients compared to HIV-negative subjects [18,19]. In a study by Peters et al, 911 subjects were analyzed in three separate cohorts, which included HIV+ patients with CD4 counts below 200, with half taking ART.…”

Section: Discussioncontrasting

confidence: 53%

Immune response to influenza A(H1N1)v in HIV-infected patients

Sansonetti

Sali

Fabbiani

et al. 2014

J Infect Dev Ctries

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Introduction: HIV infection is considered a risk factor for severe outcomes of influenza A(H1N1)v infection. However, data on immune response against influenza A(H1N1)v virus in HIV-infected patients are lacking. Methodology: Data from seven HIV-positive and 14 HIV-negative patients infected with A(H1N1)v and from 23 HIV-positive and six HIV-negative asymptomatic controls were analyzed to evaluate the clinical picture, A(H1N1)v viral shedding, and the immune response against the virus. Results: Patients displayed mainly upper respiratory tract diseases (57.1%), while pneumonia was diagnosed only in HIV-negative patients (23.8% of subjects, of which 4.8% required intensive care unit admission). At day seven, 29% of HIV-infected patients were still positive for A(H1N1)v by RT-PCR on nasopharyngeal swabs. Interestingly, a persistence of CXCL10 secretion at high level and lower IL-6 levels was observed in HIV-positive subjects. The geometric mean haemagglutination inhibition titer (HI-GMT) and anti-influenza IgM levels were lower in HIV-positive individuals while anti-influenza IgG levels remained similar in the two groups. Conclusions: The immune impairment due to HIV infection could affect A(H1N1)v clearance and could lead to a lower antibody response and a persistent secretion of CXCL10 at high levels. However, the lower IL-6 secretion and treatment with highly active antiretroviral therapy (HAART) could result in a milder clinical picture.

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“…Increased worldwide mortality was observed during the 2009 Influenza pandemics for especial groups of patients at higher risk, such as individuals immunocompromised [23,24] by cancer or transplantations [24]. Surprisingly, HIV-1-infected individuals presented a benign clinical outcome when infected by A(H1N1)pdm09 [25][26][27][28][29][30], unless when in AIDS [29]. Although Figure 5.…”

Section: Discussionmentioning

confidence: 98%

“…In contrast to the increased mortality observed in immunocompromised individuals [23], such as cancer and transplanted patients [24], affected by the emergence of influenza A(H1N1)pdm09, HIV-1-infected individuals presented benign clinical outcomes [25][26][27][28][29][30]. For instance, Barchi et al found that the clinical outcome in HIV-1-infected individuals with A(H1N1)pdm09 infection was not different from that in immunocompetent patients [25], and Ormsby et al reported that only HIV-1-infected subjects that had progressed to the immune deficiency typical of AIDS presented an increased mortality by A(H1N1)pdm09 [29].…”

Section: Introductionmentioning

confidence: 99%

HIV-1 and Its gp120 Inhibits the Influenza A(H1N1)pdm09 Life Cycle in an IFITM3-Dependent Fashion

et al. 2014

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HIV-1-infected patients co-infected with A(H1N1)pdm09 surprisingly presented benign clinical outcome. The knowledge that HIV-1 changes the host homeostatic equilibrium, which may favor the patient resistance to some co-pathogens, prompted us to investigate whether HIV-1 infection could influence A(H1N1)pdm09 life cycle in vitro. We show here that exposure of A(H1N1)pdm09-infected epithelial cells to HIV-1 viral particles or its gp120 enhanced by 25% the IFITM3 content, resulting in a decrease in influenza replication. This event was dependent on toll-like receptor 2 and 4. Moreover, knockdown of IFITM3 prevented HIV-1 ability to inhibit A(H1N1)pdm09 replication. HIV-1 infection also increased IFITM3 levels in human primary macrophages by almost 100%. Consequently, the arrival of influenza ribonucleoproteins (RNPs) to nucleus of macrophages was inhibited, as evaluated by different approaches. Reduction of influenza RNPs entry into the nucleus tolled A(H1N1)pdm09 life cycle in macrophages earlier than usual, limiting influenza's ability to induce TNF-α. As judged by analysis of the influenza hemagglutin (HA) gene from in vitro experiments and from samples of HIV-1/A(H1N1)pdm09 co-infected individuals, the HIV-1-induced reduction of influenza replication resulted in delayed viral evolution. Our results may provide insights on the mechanisms that may have attenuated the clinical course of Influenza in HIV-1/A(H1N1)pdm09 co-infected patients during the recent influenza form 2009/2010.

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Pandemic influenza A (H1N1) in HIV-1-infected patients

Abstract: HIV patients infected by the new influenza A pandemic (H1N1) virus behave similarly to the general population.

Cited by 18 publications

References 3 publications

Comparison of Influenza and SIV Specific CD8 T Cell Responses in Macaques

Comparison of Influenza and SIV Specific CD8 T Cell Responses in Macaques

Immune response to influenza A(H1N1)v in HIV-infected patients

HIV-1 and Its gp120 Inhibits the Influenza A(H1N1)pdm09 Life Cycle in an IFITM3-Dependent Fashion

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