eISSN: 1644-4124
ISSN: 1426-3912
Central European Journal of Immunology
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vol. 49
Clinical immunology

HLA class II DRB1, DQA1, DQB1 loci in patients with HIV infection and tuberculosis in a Latvian cohort group

Alena Soha
Inga Azina
Baiba Rozentale
Ksenija Kramicha
Gunta Sture
2, 4
Oksana Savicka
Galina Titovica

  1. Doctoral studies, Riga Stradins University, Riga, Latvia
  2. Latvian Centre of Infectious Disease, Riga East University Hospital, Riga, Latvia
  3. Postdoctoral studies, Riga Stradins University, Riga, Latvia
  4. Department of Internal Diseases of Riga East University Hospital, Riga Stradins University, Riga, Latvia
  5. Infectology Centre of Latvia, National Microbiology Reference Laboratory, Riga East Clinical University Hospital, Riga, Latvia
  6. Daugavpils Regional Hospital, Daugavpils, Latvia
Cent Eur J Immunol 2024; 49 (1): 37-44
Online publish date: 2024/04/19
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Until the COVID-19 pandemic, tuberculosis (TB) was the leading cause of death from a single infectious agent, ranking above HIV/AIDS. It is also the key cause of death among people infected with HIV. Tuberculosis incidence in Latvia has decreased by 25% during the last 30 years, but the mortality level of TB remains significant. The HLA class II genes are responsible for antigen presentation and regulation of immune responses, which plays an important role in individual susceptibility to infection disease. Whether or not differential HLA polymorphism contributes to TB with HIV infection and TB without HIV infection in Latvian patients is unknown.

Material and methods:
For the detection of HLA class II DQA1, DQB1, and DRB1 alleles a total of 616 subjects were enrolled, including 80 primary active TB (PATB) patients, 168 HIV-1/TB patients, 168 HIV-1 patients and 200 HC individuals.

For immunodeficiency caused by TB, HIV-1 or HIV-1/TB coinfection, alleles DRB1*12:01, 14:01, 16:01, DQA1*01:02, 01:03, 02:01, 06:01, DQB1*03:03, 06:01 are identified as protective, but DRB1*07:01, 11:01, 15:01, DQA1*02:01, 03:01, DQB1*03:01, 05:01 are identified as risk alleles.

The results of our experimental pilot studies demonstrated that HLA class II genes may contribute to the genetic risk of TB and HIV-1/TB co-infection, possibly by reducing the presentation of protective Mycobacterium tuberculosis antigens to T-helpers. It is necessary to conduct repetitive, multicentre, and large sample studies in order to draw more scientific conclusions and to confirm the relationship between TB, HIV and HIV-1/TB co-infection susceptibility and gene polymorphisms.


tuberculosis, HIV-1, HLA class II, HLA polymorphism

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