Hanuš Rozsypal

Antiretroviral Treatment of HIV Infection Does Not Influence HIVSpecific Immunity but Has an Impact on Non-Specific Immune Activation

HIV-specific and non-specific immune responses are crucial in the immunopathogenesis of HIV infection. Therefore, the objective of our study was to analyse the frequency and functional status of HIV-specific CD8+ T cells and the expression of non-specific activation markers on CD8+ T cells in HIV+ patients, and to assess the effects of combined antiretroviral treatment (cART). We examined 28 HIV+ patients, including 13 patients not receiving therapy and 15 patients on cART therapy using ELISpot assay and flow cytometry with intracellular and MHC tetramer staining. MHC tetramers detected HIV-specific CD8+ T cells in 6 HIV+ patients on cART and in 7 untreated individuals; the ELISpot method detected these cells in 5 untreated HIV+ individuals only. Reduced intracellular IFN-γ and IL-2 production by HIV-specific CD8+ T cells was detected in both treated and untreated HIV+ patients, and multifunctional CD8+ T cells simultaneously producing these cytokines were not found in any patient. In contrary to these findings, the percentage of CD8+ T cells expressing CD38 and HLA-DR was significantly higher in untreated patients as compared to HIV+ patients on cART. Together, these results suggest that the alterations of HIV-specific immunity are not influenced by the therapy of HIV infection; whereas, the non-specific chronic immune activation is down-regulated by cART.

Bilateral Holmes–Adie syndrome as an early manifestation of the HIV neuropathy

A 38-year-old HIV-1 infected woman affected with bilateral tonic pupils. Ophthalmologic examination confirmed Holmes–Adie syndrome (HAS), and peripheral distal polyneuropathy, orthostatic hypotension and leg hyperhidrosis were detected on further workup. The HAS can be either idiopathic or associated with neuropathy of various etiology (autoimmune, paraneoplastic and infectious). In our patient, the pupillotonia was the first and early symptom of hitherto unrecognized HIV neuropathy. HAS has been previously observed in association with syphilis, Lyme borreliosis, herpes simplex and parvovirus B19 infection. Our case is the first report of HAS in a case of HIV infection.

Prevalence and Incidence of Toxoplasma Infection in HIV-Positive Patients in the Czech Republic

TOXOPLASMOSIS is a major opportunistic infection infecting approximately 30% of the Czech general population (Petersen, Pollak, and Reiter-Owona, 2001). In people with latent toxoplasmosis, who subsequently become infected with HIV, the Toxoplasma infection in the latent form proceeds as such. Less frequently, a patient is first infected with HIV and then with Toxoplasma. However, deterioration of the immune system (usually with a decline of CD4 T-lymphocyte counts under 100/ml) can result in recrudescence of latent infection along with the development of clinically manifest toxoplasmic encephalitis or extracerebral toxoplasmosis. Since toxoplasmosis in HIV patients is a dynamic process, sometimes gradual and other times overtly progressive, only a single examination might not be sufficient. A long-term follow-up is necessary for understanding antibody responses and its relation to clinical and epidemiological parameters. In our study, we had the unique opportunity of following the serological and clinical parameters of 626 patients (i.e. 71% of all Czech HIV-infected persons) from 1988 to 2006 (Pospı́šilová et al. 1997; Sýkora, Zástěra, and Staňková, 1992). Hence we compared the prevalence and incidence data of these patients with the situation in the general population and point out the risks of Toxoplasma infection.

The Effect of Latent Toxoplasma gondii Infection on the Immune Response in HIV-Infected Patients

A relationship between latent toxoplasmosis and the immune system during HIV disease is poorly understood. Therefore, the aim of this follow-up study was to characterize immunological parameters in HIV-infected patients with latent toxoplasmosis and noninfected individuals. A total of 101 HIV-infected patients were enrolled in the study. The patients were classified into two groups based on anti-Toxoplasma gondii antibodies: a group of 55 toxoplasma-positive persons (TP) and a group of 46 toxoplasma-negative persons (TN). Absolute counts of several lymphocyte subsets decreased in the TP group, namely, T cells (p = 0.007), B cells (p = 0.002), NK cells (p = 0.009), CD4 T cells (p = 0.028), and CD8 T cells (p = 0.004). On the other hand, the percentage of CD8 T cells expressing CD38 and HLA-DR significantly increased during the follow-up in the TP group (p = 0.003, p = 0.042, resp.) as well as the intensity of CD38 and HLA-DR expression (MFI) on CD8 T cells (p = 0.001, p = 0.057, resp.). In the TN group, analysis of the kinetics of immunological parameters revealed no significant changes over time. In conclusion, the results suggest that latent T. gondii infection modulates the immune response during HIV infection.

Acute Appendicitis as a Manifestation of the Immune Reconstitution Inflammatory Syndrome

Acute appendicitis as a manifestation of the immune reconstitution inflammatory syndrome is repeatedly discussed in the literature, but only a few cases of acute appendicitis associated with the initiation of cART have been published as yet. We describe a case of a young HIV-infected man who suffered from acute appendicitis early after the successful switch of a failing cART regimen.

Toxic Shock Syndrome and Persistent Immune Activation in an HIVPositive Patient

The case of an HIV-positive treatment-naive male with toxic shock syndrome (TSS) is presented herein. The course of TSS was favorable; however, the patient had extremely high plasma levels of MCP-1 and CD38 and HLA-DR expression on CD8+ T cells during the acute illness. Furthermore, the numbers of CD8+ T cells were reduced and CD4+ T cells remained stable during acute illness in comparison to baseline values. MCP-1 and HLA-DR gradually decreased, but they were still elevated after a month, whereas the number of circulating CD8+ T cells increased more than fivefold. CD38 expression remained stable during this period. A further decrease in CD38, HLA-DR and MCP-1 was noted five months after the initiation of antiretroviral therapy.