Out of the 463 study participants enrolled in this study, 184 (39.7%) tested positive for H. pylori infection while 279 (60.3%) did not have the infection (Fig. 1). Among the H. pylori-infected participants, 125 (67.9%) were HIV-positive and 59 (32.1%) were HIV-negative. Among the H. pylori-negative participants, 163 (58.4%) were HIV-positive, while 116 (41.6%) were HIV negative.

Socio-demographic characteristics

The socio-demographic characteristics of the study participants are presented in Table 1. There were an equal proportion of male and female participants in this study, and nearly half of the H. pylori-infected participants being female in both HIV-positive and HIV-negative groups. The study participants ranged in age from 18 to 74 years, with a mean age of 37.2 years, and the majority fell within the 31–50 years age category in all four of group participants. Majority of the study participants were resident of urban areas (369/463, 79.7%), single (234/463, 50.5%) and had normal BMI (298/463, 64.4%) with similar proportions observed across all four groups regardless of HIV and H. pylori infection status. Interestingly, HIV/H. pylori co-infected individuals had a lower mean BMI (18.2 ± 2.4) compared to those with only H. pylori infection (21.9 ± 2.5). Most of the study participants had an education level of elementary school or less with virtually similar proportions among the four groups, while 53.1% (246/463) were employed and 42.1% (195/463) had low monthly income (Table 1).

Table 1 Socio-demographic and clinical characteristics of the study participantsCharacteristics of clinical, immunological, and virological parameters

The clinical severity of HIV infection among the HIV-positive participants was determined based on WHO guidelines. Nearly half of them (137/288, 47.6%) were categorized as clinical stage I, with around one-third (90/288, 31.3%) classified as stage II (Table 2). The remaining participants were classified as stage III and IV. We found that most of both HIV/H. pylori co-infected (81/125, 64.8%) and non-co-infected HIV-positive participants (114/163, 69.9%) were on ART therapy, with the remaining being ART-naïve. The duration of ART ranged from 6 months to 20 years, with a mean (± SD) duration of 3.2 years (± 2.5), and the majority of participants (122/195, 62.6%) received therapy for less than 3 years (Table 2).

Table 2 Clinical, immunological, and virological parameters of the study participants

The CD4+ T cell count and HIV-1 viral load, which are the most important indicators used to monitor HIV disease progression, were measured from only certain numbers of participants. The CD4+ T cell count measurement was done on 176 HIV-positive (88 ART-naïve and 88 on ART) and 88 HIV-negative individuals; mean ± SD: 518 ± 278. HIV-1 viral load quantification was performed only on the 176 HIV-positive participants (88 ART-naïve and 88 on ART), and the overall median (IQR) viral load was 11,881 copies/mL (151–201,874) (Table 2). As expected, HIV-positive patients had a significantly lower CD4+ T cell count (mean ± SD; 361 ± 191) compared to HIV-negative individuals (831 ± 106), p < 0.0001 (Table 2; Additional file 1: Fig. S1A). All HIV-negative participants had over 500 CD4+ T cells/µL, while the majority of ART-naïve (77/88, 87.5%) and ART-treated (51/88, 57.9%) HIV-positive patients had a CD4+ T cell count of 500/µL or lower (Table 2).

HIV-positive patients who received ART had a higher CD4+ T cell count (p < 0.0001) and lower viral load (p < 0.0001) compared to the ART-naïve individuals (Additional file 1: Fig. S1A, B). The inverse relationship between CD4+ T cell count and HIV-1 viral load in HIV-positive patients was also determined by Spearman’s correlation test (rs =—0.8695, p < 0.0001) (Additional file 1: Fig. S2). HIV-1 viral load was then stratified into three categories: < 10,000, 10,000–100,000, and > 100,000 copies/mL (Table 2). Most of the ART-naïve participants (51/88, 58%) had a viral load above 100,000 copies/mL, while 23.8% (21/88) of them had a viral load between 10,000 and 100,000 copies/mL. In contrast, the majority of ART-treated participants (69/88, 78.4%) had a viral load below 10,000 copies/mL (Table 2). The findings align with the expected outcomes of ART in suppressing viral replication and restoring immune function.

H. pylori infection was associated with higher CD4+ T cell count and lower HIV-1 viral load in HIV/H. pylori co-infected patients

To investigate the effect of H. pylori infection on immunological and virological parameters dynamics, we compared CD4+ T cell count and HIV-1 viral load between H. pylori infected and uninfected participants. The present study found that H. pylori-infected patients had significantly higher CD4+ T cell count compared to those without H. pylori infection in both HIV-positive (mean ± SD; 405 ± 193 versus 318 ± 180; p = 0.0006) and HIV-negative (870 ± 124 versus 794 ± 66; p = 0.0024) participants (Fig. 2A). The association between H. pylori infection and higher CD4+ T cell count remained consistent across ART-naïve (p = 0.002) and ART-received (p = 0.0406) HIV-positive participants (Fig. 2B). Thus, this study provides evidence supporting the association between H. pylori infection and higher CD4+ T cell counts in HIV-positive participants, regardless of ART status.

Fig. 2

Effect of H. pylori infection on CD4 + T cell count. A Comparison of CD4+ T cell count between H. pylori-negative (HP-) and-positive (HP +) groups among HIV-negative (HIV-) and-positive (HIV +) study participants. B Comparison of CD4+ T cell count between HP- and HP + groups among ART-Naïve or on ART HIV-positive participants. n = 44 per group. Mean ± SD of CD4+ T cell counts (cells/µL) are shown. p values between the two groups were determined using the unpaired t-test; *p < 0.05; **p < 0.01; ***p < 0.001; ****p < 0.001

In addition, we assessed the association of H. pylori infection with HIV-1 viral load among HIV-positive participants. Interestingly, HIV-positive individuals co-infected with H. pylori [median (IQR); 9240 copies/mL (149—111,175)] had significantly lower viral load compared to those without H. pylori infection [21,271 copies/mL (219–246,895)], p = 0.0356 (Fig. 3A). This lower HIV-1 viral load level associated with H. pylori infection was also evident in both ART-naïve and ART-received groups. Specifically, in the ART-naïve participants, those infected with H. pylori had a substantially lower HIV-1 viral load [median (IQR); 104,919 copies/mL (9911–340,043)] compared to those who were not infected [224,472 copies/mL (21,888–442,686)], p = 0.0268. Among those who received ART, the median HIV-1 viral load in H. pylori-infected individuals [149 copies/mL (IQR: 75 – 3,409)] was lower than in those uninfected participants [287 copies/mL (IQR: 94–18,613)], although the difference was not statistically significant (p = 0.0536) (Fig. 3B).

Fig. 3

Effect of H. pylori infection on HIV-1 viral load level. A Comparison of HIV-1 viral load between H. pylori-negative (HP−) and-positive (HP +) groups among HIV-positive (HIV +) study participants. B Comparison of HIV-1 viral load between HP- and HP + groups among ART-Naïve or on ART HIV-positive participants. n = 44 per group. Median HIV-1 viral loads (copies/mL) with interquartile range (IQR) are shown. p values between the two groups were determined using the Mann–Whitney test; *p < 0.05

Overall, this data shows that H. pylori co-infection was associated with higher CD4+ T cell count and reduced HIV-1 viral load in HIV-positive individuals, regardless of ART status. Linear regression analysis also confirmed that H. pylori infection was positively associated with the CD4+ T cell count [adjusted β (95% CI), 69.5 (11.7–127.4); p = 0.019], while inversely associated with the HIV-1 viral load [adjusted β (95% CI), − 20,929 (− 45,503–3,644); p = 0.094] in HIV-positive patients (Tables 3 and 4).

Table 3 Linear regression analysis of factors associated with CD4+ T cell count among HIV-positive and-negative participantsTable 4 Linear regression analysis of factors associated with HIV-1 viral load among HIV-positive participantsAssociation of socio-demographic and clinical factors with CD4+ T cell count and HIV-1 viral load

We further assessed the association of socio-demographic, economic and clinical factors with CD4+ T cell count and HIV-1 viral load parameters in HIV-positive or -negative individuals using a simple and multiple linear regression analysis and presented them in Tables 3 and 4, respectively. Socio-demographic factors, such as gender, residence area, marital status or occupation showed no significant association with CD4+ T cell count (Table 3) or HIV-1 viral load levels (Table 4) in HIV-positive individuals. Intriguingly, linear regression analysis demonstrated that khat chewing, a psychoactive substances, was associated with lower CD4+ T cell count [unadjusted β (95% CI), − 132.8 (− 222.6–− 43.0); p = 0.004] and higher HIV-1 viral loads [unadjusted β (95% CI), 146,158 (18,982–273,335), p = 0.025] in HIV-positive patients, while alcohol drinking and smoking showed no association with CD4+ T cell count and HIV-1 viral load regardless of HIV status. Clinical factors, such as BMI, ART status, and duration of therapy, were associated with higher CD4+ T cell count and lower HIV-1 viral load (Tables 3 and 4). Conversely, the WHO clinical HIV stage was negatively associated with CD4+ T cell count and positively related to viral load among HIV-positive individuals (Tables 3 and 4).