scholarly journals Clinical and immunological features of psoriasis vulgaris in HIV-infected patients

2022 ◽  
pp. 94-101
Author(s):  
E. Yu. Evdokimov ◽  
Zh. B. Ponezheva ◽  
E. V. Svechnikova ◽  
A. V. Sundukov

Introduction. Psoriasis is an inflammatory dermatosis, which has characteristic clinical features and is closely associated with immunological changes in the skin. HIV-infected patients suffering from psoriasis have immunological features associated with the effect of HIV virus on CD4+T-lymphocytes.Aim. To identify clinical features of psoriasis in HIV-infected patients depending on the stage of HIV infection and immune status.Materials and methods. An open prospective study (2014–2018) included 143 patients with psoriasis vulgaris, of which 79 (55.2%) were infected with HIV and 64 (44.8%) were not infected with HIV. The groups were comparable in terms of age and gender. The diagnosis of psoriasis vulgaris was established with due account for its clinical presentation and histologically confirmed in 29 (20.3%) patients, of which 17 (58.6%) were infected with HIV and 12 (41.4%) were not infected with HIV. In a biopsy, tissue samples were taken from the areas of inflammatory and healthy skin in each patient. Numbers of CD4+ and CD8+T-lymphocytes in the biopsy samples obtained were calculated using immunohistochemical staining of biopsy. The severity of psoriasis progress was assessed using the psoriasis lesions severity index, taking into account the body surface area covered by lesions, the intensity of erythema, infiltration and sloughing of skin. In the course of the study, the patients had general clinical examinations performed, their HIV infection confirmed or denied, their immune status assessed, and their clinical stage of HIV infection determined.Results and discussion. Mild psoriasis was less often identified, and moderately severe and severe psoriasis was more often observed in HIV-infected patients as compared to HIV-negative patients. The psoriatic plaque CD8+T-lymphocyte counts in HIV-infected patients grew with increasing immunosuppression and clinical stage of HIV infection; these changes were not observed in HIV-negative patients.Сonclusion. HIV-infected patients often have moderately severe (39.2%) and severe (22.8%) psoriasis vulgaris. The psoriatic plaque CD8+T-lymphocyte counts in HIV-infected patients predominate over the CD4+T-lymphocyte counts, while the HIV-negative patients show the opposite test results.

2019 ◽  
Vol 13 (1) ◽  
pp. 59-64
Author(s):  
Tommy Mlambo ◽  
Mqondisi Tshabalala ◽  
Tsitsi Bandason ◽  
Kudakwashe Mhandire ◽  
Bonface Mudenge ◽  
...  

Introduction: In response to the human immunodeficiency virus (HIV) infection, activated immune cells produce several cytokines that alter the immune response and HIV disease progression. We quantified Th1/Th2/Th17 cytokines in an antiretroviral therapy naïve (ART) cohort to investigate their correlation with traditional markers of HIV disease progression; CD4+ T-lymphocytes and virus load (VL). Methods: We enrolled 247 HIV-infected ART-naïve participants into the study. CD4+ T- and CD8+ T-lymphocytes were enumerated using flow cytometry. VL was quantified using the Cavidi ExaVirTM Load assay. IL-2, IL-4, IL-6, IL-10, IL-17A, TNF-α, and IFN-γ levels were quantified using the BD Cytometric Bead Array Human Th1/Th2/Th17 cytokine assay. The Kendall’s rank correlation coefficient was used to determine the correlation between log10 transformed data for cytokine levels and CD4+ T- and CD8+ T-lymphocytes, CD4/CD8 ratio, and VL. Results: The median CD4+ T- and CD8+ T-lymphocyte counts were 458 cells/µL (IQR:405-556) and 776 cells/µL (IQR:581-1064), respectively. The median CD4/CD8 ratio was 0.6 (IQR: 0.45-0.86). The median VL was log103.3.copies/mL (IQR:2.74-3.93). Low CD4+ T-lymphocyte counts (p=0.010) and CD4/CD8 ratio (p=0.044) were significantly correlated with high VL. There was no significant correlation of cytokine levels with CD4+ T-, CD8+ T-lymphocyte counts and CD4/CD8 ratio. However, high levels of IL-17A (p=0.012) and IL-6 (p=0.034) were significantly correlated with high VL. Conclusion: Our study contributes to the little knowledge available on the role of cytokine profiles in the immune response to subtype C HIV infection.


Author(s):  
I Made Sila Darmana ◽  
Endang Retnowati ◽  
Erwin Astha Triyono

Measuring HIV p24 protein is a test which is more practical than determination of CD4+ T-lymphocyte counts and viral load, as it does not require a very sophisticated instrument and requires a lower cost. Independent predictive value of p24 to the decline of CD4+ T-lymphocytes, clinical progression and survival in HIV-infected patients have been reported. In this study, HIV-infected patients were found to have HIV p24 protein levels inversely proportional to CD4+ T-lymphocyte counts by using Spearman test (R2=0.225; p=0.0331). Studies on the correlation between HIV p24 protein levels and CD4+ T-lymphocyte counts in stage I HIV infection have not yet been reported. The aim of this study was to prove the correlation between HIV p24 protein levels and CD4+ T-lymphocytes in stage I HIV infection. Research issue was whether a correlation between HIV p24 protein levels and CD4+ T-lymphocyte counts in stage I HIVinfection existed ? The hypothesis was that a correlation between HIV p24 protein levels and CD4+ T-lymphocyte counts in stage I HIV infection existed. The study design was cross sectional observational. Subjects consisted of 30 stage I HIV-infected patients treated at the Infectious Disease Intermediate Care Unit, Dr. Soetomo Hospital and VCT Clinic of the Dr. Ramelan Naval Hospital, Surabaya from May to July 2014. Stage I HIV infection is an asymptomatic HIV infection or with persistent generalized lymphadenopathy and the patient is able to perform normal activities. Levels of p24 were measured by ELISA method and CD4+ T-lymphocyte counts using flowcytometry(BD FACSCaliburTM). The results were statistically analyzed using Pearson’s correlation test. HIV p24 protein levels in stage I of HIV infection ranged from 1.8 to 10.8 pg/mL, mean of 5.14 pg/mL and a standard deviation of 2.08 pg/mL. CD4+ T-lymphocyte counts decreased with a range of 49-559 cells /uL for absolute values and 4.42–26.02% for percentage values Correlations between blood p24 levels and CD4+ T-lymphocyte counts either absolute (r=–0.392, p=0.032) or percentage (r=–0.363, p=0.049) were found. In stage I HIV-infected patients, a negative correlation was found between p24 levels and CD4+ T-lymphocyte counts, in both CD4+T-lymphocyte counts as absolute and as well as percentage values. This negative correlation showed that the p24 HIV levels were inversely proportional to the CD4+ T-lymphocyte counts. HIV p24 protein levels have a possibility to be used predicting CD4+ T-lymphocyte counts


2019 ◽  
Vol 77 (5) ◽  
pp. 357-365 ◽  
Author(s):  
Omar Herrera Vazquez ◽  
Matthew L. Romo ◽  
Agnès Fleury

ABSTRACT Infections caused by the human immunodeficiency virus (HIV) and by the larvae of Taenia solium (i.e., cysticercosis) are still widespread in many developing countries. Both pathologies modify host immune status and it is possible that HIV infection may modulate the frequency and pathogeny of cysticercosis of the central nervous system (i.e., neurocysticercosis [NCC]). Objective: To describe published cases of NCC among HIV-positive patients and to evaluate whether the characteristics of NCC, including frequency, symptoms, radiological appearance, and response to treatment differed between HIV-positive and HIV-negative patients. Methods: Forty cases of NCC/HIV co-infected patients were identified in the literature. Clinical and radiological characteristics, as well as response to treatment, were compared with non-matching historical series of NCC patients without HIV infection. Results: Most of these patients had seizures and multiple vesicular parasites located in parenchyma. Clinical and radiological characteristics were similar between HIV-positive and HIV-negative patients with NCC, as well as between immunocompromised and non-immunocompromised HIV-positive patients. Conclusion: Our review did not reveal clear interactions between HIV and NCC. This may be partially due to the small number of cases and reliance on published research. A systematic, multi-institutional effort aiming to report all the cases of this dual pathology is needed to confirm this finding and to clarify the possible relationship between both pathogens.


2006 ◽  
Vol 81 (1) ◽  
pp. 74-83 ◽  
Author(s):  
Avi-Hai Hovav ◽  
Mark J. Cayabyab ◽  
Michael W. Panas ◽  
Sampa Santra ◽  
John Greenland ◽  
...  

ABSTRACT The most promising vaccine strategies for the induction of cytotoxic-T-lymphocyte responses have been heterologous prime/boost regimens employing a plasmid DNA prime and a live recombinant-vector boost. The priming immunogen in these regimens must elicit antigen-specific memory CD8+ T lymphocytes that will expand following the boosting immunization. Because plasmid DNA immunogens are expensive and their immunogenicity has proven disappointing in human clinical trials, we have been exploring novel priming immunogens that might be used in heterologous immunization regimens. Here we show that priming with a prototype recombinant Mycobacterium smegmatis strain expressing human immunodeficiency virus type 1 (HIV-1) gp120-elicited CD4+ T lymphocytes with a functional profile of helper cells as well as a CD8+ T-lymphocyte population. These CD8+ T lymphocytes rapidly differentiated to memory cells, defined on the basis of their cytokine profile and expression of CD62L and CD27. Moreover, these recombinant-mycobacterium-induced T lymphocytes rapidly expanded following boosting with a recombinant adenovirus expressing HIV-1 Env to gp120-specific CD8+ T lymphocytes. This work demonstrates a remarkable skewing of recombinant-mycobacterium-induced T lymphocytes to durable antigen-specific memory CD8+ T cells and suggests that such immunogens might be used as priming vectors in prime/boost vaccination regimens for the induction of cellular immune responses.


2014 ◽  
Vol 4 (6) ◽  
pp. 495-501 ◽  
Author(s):  
Nathalie Gabra ◽  
Saud Alromaih ◽  
Leandra Mfuna Endam ◽  
Rose Marie Brito ◽  
Françoise Larivière ◽  
...  

2012 ◽  
Vol 58 (5) ◽  
pp. 394-397
Author(s):  
P. G. D. Navaneethapandian ◽  
R. Karunaianantham ◽  
S. Subramanyan ◽  
P. Chinnayan ◽  
P. Chandrasekaran ◽  
...  

2003 ◽  
Vol 71 (7) ◽  
pp. 3920-3926 ◽  
Author(s):  
Zhen Li ◽  
C. Marcela Díaz-Montero ◽  
Gustavo Valbuena ◽  
Xue-Jie Yu ◽  
Juan P. Olano ◽  
...  

ABSTRACT The 1.2-kb DNA fragment of the Rickettsia conorii outer membrane protein B gene (OmpB451-846) was subcloned using site-specific PCR primers and expressed as six smaller fragments: OmpB458-652, OmpB595-744, OmpB595-654, OmpB645-692, OmpB689-744, and OmpB739-848. NCTC cells transfected with a mammalian expression vector expressing the fragments OmpB689-744 and OmpB739-848 stimulated immune anti-R. conorii CD8 T lymphocytes, suggesting the presence of CD8 T-lymphocyte-stimulating epitopes on these fragments. In order to further characterize the CD8 T-lymphocyte-stimulatory elements, CD8 T-lymphocyte epitopes on OmpB689-744 and OmpB739-848 were mapped by overlapping synthetic peptides. The ability of these synthetic peptides to stimulate immune CD8 T lymphocytes was determined by gamma interferon (IFN-γ) production and cell proliferation after incubation with simian virus 40-transformed murine vascular endothelial cells in the presence of a 20 μM solution of each synthetic peptide. Five synthetic peptides, SKGVNVDTV (OmpB708-716), ANVGSFVFN (OmpB735-743), IVSGTVGGQ (OmpB749-757), ANSTLQIGG (OmpB789-797), and IVEFVNTGP (OmpB812-820), induced secretion of IFN-γ at significantly higher levels than the controls. Three of these five peptides, SKGVNVDTV (OmpB708-716), ANSTLQIGG (OmpB789-797), and IVEFVNTGP (OmpB812-820), also stimulated the proliferation of immune CD8 T lymphocytes. Significantly higher levels of specific cytotoxic T-lymphocyte killing were observed with the same three synthetic peptides, SKGVNVDTV (OmpB708-716), ANSTLQIGG (OmpB789-797), and IVEFVNTGP (OmpB812-820).


Author(s):  
I Made Sila Darmana ◽  
Endang Retnowati ◽  
Erwin Astha Triyono

Measuring HIV p24 protein is a test which is more practical than determination of CD4+ T-lymphocyte counts and viral load, asit does not require a very sophisticated instrument and requires a lower cost. Independent predictive value of p24 to the decline ofCD4+ T-lymphocytes, clinical progression and survival in HIV-infected patients have been reported. In this study, HIV-infected patientswere found to have HIV p24 protein levels inversely proportional to CD4+ T-lymphocyte counts by using Spearman test (R2=0.225;p=0.0331). Studies on the correlation between HIV p24 protein levels and CD4+ T-lymphocyte counts in stage I HIV infection have notyet been reported. The aim of this study was to prove the correlation between HIV p24 protein levels and CD4+ T-lymphocytes in stageI HIV infection. Research issue was whether a correlation between HIV p24 protein levels and CD4+ T-lymphocyte counts in stage I HIVinfection existed ? The hypothesis was that a correlation between HIV p24 protein levels and CD4+ T-lymphocyte counts in stage I HIVinfection existed. The study design was cross sectional observational. Subjects consisted of 30 stage I HIV-infected patients treated at theInfectious Disease Intermediate Care Unit, Dr. Soetomo Hospital and VCT Clinic of the Dr. Ramelan Naval Hospital, Surabaya from Mayto July 2014. Stage I HIV infection is an asymptomatic HIV infection or with persistent generalized lymphadenopathy and the patientis able to perform normal activities. Levels of p24 were measured by ELISA method and CD4+ T-lymphocyte counts using flowcytometry(BD FACSCaliburTM). The results were statistically analyzed using Pearson’s correlation test. HIV p24 protein levels in stage I of HIVinfection ranged from 1.8 to 10.8 pg/mL, mean of 5.14 pg/mL and a standard deviation of 2.08 pg/mL. CD4+ T-lymphocyte countsdecreased with a range of 49-559 cells /uL for absolute values and 4.42–26.02% for percentage values Correlations between blood p24levels and CD4+ T-lymphocyte counts either absolute (r=–0.392, p=0.032) or percentage (r=–0.363, p=0.049) were found. In stageI HIV-infected patients, a negative correlation was found between p24 levels and CD4+ T-lymphocyte counts, in both CD4+T-lymphocytecounts as absolute and as well as percentage values. This negative correlation showed that the p24 HIV levels were inversely proportionalto the CD4+ T-lymphocyte counts. HIV p24 protein levels have a possibility to be used predicting CD4+ T-lymphocyte counts.


Pathobiology ◽  
2021 ◽  
pp. 1-12
Author(s):  
Omar Bushara ◽  
Katrina Krogh ◽  
Samuel Edward Weinberg ◽  
Brian Steven Finkelman ◽  
Leyu Sun ◽  
...  

<b><i>Background:</i></b> Anal squamous cell carcinoma (SCC) is a rare gastrointestinal malignancy with rising incidence, both in the United States and internationally. The primary risk factor for anal SCC is human papillomavirus (HPV) infection. However, there is a growing burden of disease in patients with human immunodeficiency virus (HIV) and HPV coinfection, with the incidence of anal SCC significantly increasing in this population. This is particularly true in HIV-infected men. The epidemiologic correlation between HIV-HPV coinfection and anal SCC is established; however, the immunologic mechanisms underlying this relationship are not well understood. <b><i>Summary:</i></b> HIV-related immunosuppression due to low circulating CD4+ T cells is one component of increased risk, but other mechanisms, such as the effect of HIV on CD8+ T lymphocyte tumor infiltration and the PD-1/PD-L1 axis in antitumor and antiviral response, is emerging as significant contributors. The goal of this article is to review existing research on HIV-HPV coinfected anal SCC and precancerous lesions, propose explanations for the detrimental synergy of HIV and HPV on the pathogenesis and immunologic response to HPV-associated cancers, and discuss implications for future treatments and immunotherapies in HIV-positive patients with HPV-mediated anal SCC. <b><i>Key Messages:</i></b> The incidence of anal squamous cell carcinoma is increased in human immunodeficiency virus (HIV)-infected patients, even in patients on highly active antiretroviral therapy. Locoregional HIV infection may enhance human papillomavirus oncogenicity. Chronic inflammation due to HIV infection may contribute to CD8+ T lymphocyte exhaustion by upregulating PD-1 expression, thereby blunting cytotoxic antitumor response.


Author(s):  
W. Curry

Programmed Cell Death – 1 (PD1) inhibition activates tumor-specific T-lymphocytes and is an effective clinical therapy against some cancers. Preclinical data regarding immune checkpoint inhibitors against malignant glioma is scant, and interim analyses of clinical trials suggest modest effect in patients as single agents. We examined PD-1 inhibition in murine glioblastoma models in combination with other immunomodulatory agents. Methods – Syngeneic glioma tumors (GL261 and CT2A) were implanted intracranially in C57/Bl6 mice. In separate experiments, PD-1 inhibition was combined with antibody blockade of t-cell immunoglobulin and mucin protein (TIM3), ligation of OX40 on T-lymphocytes, or vaccination with irradiated GM-CSF expressing tumor cells. Systemic antitumor immunity and tumor infiltrating lymphocytes were analyzed by ELISPOT assay and flow cytometry, respectively. Results - In both syngeneic glioma models, day 3,6, and 9 systemic delivery of a monoclonal antibody against PD-1 led to increased survival vs. controls. In animals with GL261 intracranial tumors, survival was improved by combination of PD-1 blockade with subcutaneous injection of irradiated GM-CSF expressing GL261 tumor cells, with antibody blockade of t-cell immunoglobulin and mucin protein 3 (TIM3), or binding of OX40 on T-lymphocytes by an activating antibody. In most cases, ELISPOT analyses demonstrated enhanced Th1 immunity by combination immunotherapies. Vaccination was associated with an increased intratumoral CD8+ T lymphocyte / FoxP3+ T lymphocyte ratio. Conclusion –Blockade of PD-1 on T lymphocytes in glioma-bearing mice is active. Both antitumor immunity and survival can be enhanced by combination of PD-1 inhibition with agents that activate antitumor immunity by complementary mechanisms.


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