scholarly journals COVID-19 Vaccines for HIV-Infected Patients

Viruses ◽  
2021 ◽  
Vol 13 (10) ◽  
pp. 1890
Author(s):  
Maria M. Plummer ◽  
Charles S. Pavia

Nearly 40 years have passed since the initial cases of infection with the human mmunodeficiency virus (HIV) were identified as a new disease entity and the cause of acquired immunodeficiency disease (AIDS). This virus, unlike any other, is capable of causing severe suppression of our adaptive immune defense mechanisms by directly infecting and destroying helper T cells leading to increased susceptibility to a wide variety of microbial pathogens, especially those considered to be intracellular or opportunistic. After T cells are infected, HIV reproduces itself via a somewhat unique mechanism involving various metabolic steps, which includes the use of a reverse transcriptase enzyme that enables the viral RNA to produce copies of its complementary DNA. Subsequent physiologic steps lead to the production of new virus progeny and the eventual death of the invaded T cell. Fortunately, both serologic and molecular tests (such as PCR) can be used to confirm the diagnosis of an HIV infection. In the wake of the current COVID-19 pandemic, it appears that people living with HIV/AIDS are equally or slightly more susceptible to the etiologic agent, SARS-CoV-2, than the general population having intact immune systems, but they may have more serious outcomes. Limited clinical trials have also shown that the currently available COVID-19 vaccines are both safe and effective in affording protection to HIV/AIDS patients. In this review, we further explore the unique dynamic of HIV/AIDS in the context of the worldwide COVID-19 pandemic and the implementation of vaccines as a protective measure against COVID-19, as well as what immune parameters and safeguards should be monitored in this immunocompromised group following vaccination.

2019 ◽  
Vol 2019 ◽  
pp. 1-7 ◽  
Author(s):  
J. K. Kirinyet

Background. Malaria and HIV/AIDS infections are among the major public health concerns in sub-Saharan Africa, where they are associated with high morbidity and mortality. Recent findings indicate that individual people living with HIV/AIDS (PLWHA) with lower levels of CD4 T-cell count below 200/mm3 tend to experience higher mean malaria parasite densities than their counterparts with higher CD4 T-cells counts. Aim. The study was conducted to assess the pattern of malaria parasite density at different levels of CD4 T-cells among people living with HIV/AIDS in Western part of Kenya. Subjects and Methods. A randomized antimalarial treatment study among 126 people living with HIV/AIDS was conducted at Chulaimbo Sub-County Hospital, Western Kenya. All the participants enrolled into the study had their blood samples assessed for malaria parasite densities before commencement of antimalarial therapy and the results correlated with their CD4 T-cells levels obtained from their respective files. Results. Mean malaria parasite density on pretreatment samples was 43,168 parasites /μL of blood, median was 17,720, and mode was 4,000. Male participants had a higher geometrical mean parasite density (26,424) compared to females’ (15,346) (p = 0.03). Low CD4 counts were associated with high density malaria parasitaemia and consequently, very high CD4 counts seemed to exhibit low malaria parasite density among PLWHA. An insignificant negative correlation, however, between CD4 T-cells count and malaria parasite densities was noted (p = 0.169). Conclusion. The study was able to establish higher parasite density among individuals with ≤200 cells/μL than their counterparts with >200 cells/μL of CD4 T-cell levels in PLWHA resident in Western Kenya. Secondly, males significantly had a higher geometrical mean parasite density than females regardless of their CD4 status. It is anticipated that the results from this study could be used/applied in developing interventional measures to address malaria/HIV-AIDS coinfections aimed at saving life, particularly in the sub-Saharan African region where the two infections are rampant.


2010 ◽  
Vol 78 (6) ◽  
pp. 2723-2733 ◽  
Author(s):  
Kaitian Peng ◽  
Denise M. Monack

ABSTRACT Upon microbial challenge, organs at various anatomic sites of the body employ different innate immune mechanisms to defend against potential infections. Accordingly, microbial pathogens evolved to subvert these organ-specific host immune mechanisms to survive and grow in infected organs. Francisella tularensis is a bacterium capable of infecting multiple organs and thus encounters a myriad of organ-specific defense mechanisms. This suggests that F. tularensis may possess specific factors that aid in evasion of these innate immune defenses. We carried out a microarray-based, negative-selection screen in an intranasal model of Francisella novicida infection to identify Francisella genes that contribute to bacterial growth specifically in the lungs of mice. Genes in the bacterial tryptophan biosynthetic pathway were identified as being important for F. novicida growth specifically in the lungs. In addition, a host tryptophan-catabolizing enzyme, indoleamine 2,3-dioxygenase 1 (IDO1), is induced specifically in the lungs of mice infected with F. novicida or Streptococcus pneumoniae. Furthermore, the attenuation of F. novicida tryptophan mutant bacteria was rescued in the lungs of IDO1−/− mice. IDO1 is a lung-specific innate immune mechanism that controls pulmonary Francisella infections.


2018 ◽  
Vol 12 (12) ◽  
pp. 1073-1078
Author(s):  
Amany Elkholy ◽  
Mirvat El Anany ◽  
Ghada Mohamed Ezzat ◽  
Fadwa Abd El Reheem ◽  
Assem Fouad Elessawy

Introduction: Interpreting the interactions between M. tuberculosis and the host innate and adaptive immune defense mechanisms is mandatory for understanding the pathogenesis of active pulmonary TB (APTB). The aim was to describe the distribution of mononuclear cells in APTB and their relation to disease severity. Methodology: A case-control study of peripheral blood CD4+ T cells, CD8+ T cells, B-lymphocytes, NK cells, T regulatory lymphocytes (Tregs) and monocytes by flow cytometry. The patients had clinical presentations of APTB, positive tuberculin skin tests, acid-fast bacilli smears and sputum cultures using BACTEC 960. Results: There was a significant decrease in the haemoglobin level and the absolute lymphocytic count (p < 0.01), while both the neutrophil count and erythrocyte sedimentation rate showed significant increase in the APTB patients compared to HC with p-values < 0.001 and < 0.0001 respectively. Both the CD4+/CD8+ ratio and the percentages of CD3−CD19+ cells were significantly lower in APTB patients (p = 0.03 and p = 0.005 respectively). The percentages of CD4+, CD8+, CD3−CD19+, CD14+, and CD3−CD (16+56)+ cells showed no significant differences, when comparing either disease severity groups, or cavitated and non-cavitated groups of APTB patients. There was significant increase in the CD4+25+ lymphocytes in the advanced APTB patients than in the mild disease group (p < 0.05). Conclusions: B-lymphocytes and CD4/CD8 ratios were significantly lower in the APTB patients than controls with no association with disease severity. CD4+ CD25+hi Tregs were significantly higher in the advanced versus mild groups.


2017 ◽  
Vol 8 ◽  
pp. 117991611774291 ◽  
Author(s):  
Ayan Mukherjee ◽  
Sandeep Lahiry ◽  
Anindya Mukherjee ◽  
Shouvik Choudhury ◽  
Rajasree Sinha

Aim: To explore the stigmatizing pattern in people living with HIV/AIDS (PLWHA) and assess coping strategies adopted for quality of life (QOL) appraisal. Methods: In the background of a descriptive, cross-sectional research design, PLWHA attending HIV (human immunodeficiency virus) outpatient clinic at Medical College, Kolkata (n = 120) were enrolled through “snowball sampling.” A brief semistructured interview schedule was used to elicit data on socio-demographics. Stigma was assessed using a 4-point scale (40-item). Quality of life was assessed using WHOQOL-BREF (World Health Organization Quality-of-Life) scale (26-item). Results: About 96.7% reported being stressed. Stigma was mostly confronted in socio-familial context. Fear of being stigmatized was much higher compared with those who actually faced stigma (69.2% vs 27.5%; P < .01). Quality of life negatively correlated with internalizing of stigma in the psychological domain ( P < .01). Proportion experiencing actual stigma (women vs men: 79% vs 74%) experienced an above moderate QOL. Multiple defense mechanisms were identified. “Altruism,” “Anticipation,” and “Humor” were the most preferred defense strategies. However, such coping strategies appeared to be self-taught and only modestly helpful in managing perceived stigma. Conclusions: People living with HIV/AIDS should avoid internalizing stigmatized feeling and engage in social activities to work toward a better QOL.


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