The frequency of HIV-HBsAg co-infection was 9.6% overall, according to the study, indicating a significant burden of both illnesses in the community under investigation. Compared to the 11.5% prevalence found at a different health facility in north-central Nigeria in 2012 (Tremeau-Bravard et al., 2012), the 12.5% prevalence reported in north-western Nigeria in 2013 (Hamza et al., 2013), and the 12.4% in South-South Nigeria (Okonko et al., 2020a), this prevalence is a little lower. However, it is higher than the 1.8% reported in Warri, Nigeria (Okonko et al., 2023a), 3.0%, and 3.1% reported by Okonko et al. (2023b) and Cookey et al. (2021) in Port Harcourt, Nigeria, respectively. It is also higher when compared with the 2.5%, 2.6%, and 2.7% reported in some earlier studies in Nigeria and New York, respectively (Toussi et al., 2007; Okonko et al., 2012; Mbaawuaga et al., 2014). According to statistics from separate research conducted in southwest Nigeria, the prevalence of HIV among patients in 2009 was 5.7% (Adewole et al., 2009). These results, which show regional differences in prevalence, may point to specific.
The study found that the overall prevalence of HIV-HBsAg co-infection was 46.5%, indicating a substantial burden of both infections in the studied population. This is higher than the 12.5% prevalence reported in north-western Nigeria in 2013 (Hamza et al., 2013) and the 11.5% discovered in a different health institution in north-central Nigeria in 2012 (Tremeau-Bravard et al., 2012). Also, it is higher than the 8.0% recorded in Port Harcourt, Nigeria (Okonko et al., 2023c) and the 6.3% observed in Uyo, Nigeria (Innocent-Adiele et al., 2021). These data, which indicate regional variations in prevalence, may indicate distinct epidemiological variables operating in the country and point out a hole in our current understanding of the epidemiology of HIV/HBV co-infection.
Plasmodium falciparum malaria and HIV co-infection were more common, with a frequency of 14.4%, indicating a considerable co-occurrence of both illnesses in the patient population. Furthermore, the 19.5% prevalence of HIV and malaria co-infection observed in this study supports that of Kwenti (2018) where it was found that the prevalence of Malaria and HIV coinfection in Sub-Saharan Africa was 0.7–47.5% overall.
Eighteen patients (or 9.0% of the whole group) were found to have both HIV/HBsAg and Plasmodium falciparum co-infection. Also, this 9.0% reported here for HIV/HBsAg/P. falciparum coinfections is higher than the 5.0% in an earlier study in Port Harcourt, Nigeria (Okonko et al., 2021). The prevalence of HBV and malaria co-infection among different participants has also been revealed by a few additional investigations. An HBV malaria co-infection rate was noted in a study of a similar nature conducted in Kano by Dabo et al. (2015). The findings of this study are in stark contrast to those of Sharif et al. (2016), who hypothesized that the co-infection of HBV and malaria lessens the severity of HBV and malaria when they occur alone. According to this study's findings, patients who co-infect with HBV and malaria have a higher risk of developing liver dysfunction than patients who just have one infection.
Species distribution in various regions of the nation highlights a gap in our present knowledge of the epidemiology of HIV/HBV co-infection. The prevalence of HIV- Plasmodium falciparum co-infection was even higher at 14.4%, suggesting a significant co-occurrence of these diseases in the patient population. Earlier research revealed that estimates of the prevalence of Plasmodium spp. and HBV coinfection ranged substantially, from 1.0 to 41.0% (Okonko et al., 2023b). According to Aernan et al. (2011), most (41.0%) of Plasmodium spp. and HBV coinfections were detected among Nigerian blood donors. Plasmodium spp. and HBV coinfection were estimated to be present in 6.0% of the population (Kotepui & Kotepui, 2020). Among the individuals studied here, 18(9.0%) were identified as having both HIV, HBsAg and Plasmodium falciparum co-infection. This contradicted the 0.0% reported in Port Harcourt, Nigeria (Okonko et al., 2023b), 0.5% reported in North-Central Nigeria (Omatola & Okolo, 2021) and 3.8% reported in Akure, Nigeria (Afolabi & Bakare, 2022).
Males had higher rates of HBsAg-HIV-1 co-infection than females. This finding is not consistent with earlier findings by other researchers in Port Harcourt and other parts of Nigeria (Omatola et al., 2019; Cookey et al., 2021, 2022; Okonko et al., 2022, 2023a, b). however, the findings of other previous studies were consistent with the findings of this present study (Zafrin et al., 2019; Omatola et al., 2020; Okonko et al., 2020b, 2023c). Plasmodium falciparum -HIV was found in 4 male patients (representing 7% of the whole study population and 20.9% of the male patients), compared to 25 female patients (12.5% of the entire study population and 18.8% of the female patients). Likewise, of the 18 (9.0%) patients who also had HBsAg- Plasmodium falciparum co-infection, 10.4% were males and 8.2% were females. Notably, 5.5% of the overall sample population and 61.1% of positive cases in this co-infected group of patients were female. This gender gap in co-infection rates is an intriguing discovery that could necessitate more investigation. Despite the lower number (38.9% of positive cases and 3.5% of the overall sample group), male co-infection among patients still has a significant impact.
In terms of age, the prevalence of HBsAg-HIV-1 co-infection was considerably higher in the age group ≥ 51 (54.2%) than in other age groups. This agrees favourably with previous studies (Braga et al., 2005; Kotepui & Kotepui, 2020; Afolabi & Bakare, 2022), however, this disagrees with the findings of Omatola and Okolo (2021) and Okonko et al. (2020a,b, 2023a,b) who reported a higher prevalence in the age groups below 50. It also disagrees with Okonko et al. (2020b) who reported that HBV infection only affects people in Port Harcourt, Nigeria, between the ages of 16 and 20. The prevalence of Plasmodium falciparum-HIV-1 co-infection was considerably higher in the age group ≤ 30 (26.4%) than in other age groups (with 17.8% and 18.1%). Likewise, a higher prevalence of HBsAg- Plasmodium falciparum co-infection occurred in the age group ≤ 30 (14.7%) compared to other age groups with 7.3% and 9.0%. A study by Kotepui and Kotepui (2020) revealed no significant difference between participants' ages and the risk of coinfection with Plasmodium spp. and HBV. In a study by Omatola and Okolo (2021) in North-Central Nigeria, single and concurrent infections peaked around ages 31 to 40 but decreased with older ages. In a separate study in Port Harcourt, Nigeria, Cookey et al. (2021) discovered a higher rate of HBV infection in the age group > 59 years.
The study also looked at the distribution of co-infection rates among patients with various marital situations. As a result, it was discovered that married patients had a somewhat greater percentage of co-infection cases (38.9%), followed by single patients (44.4%). Patients who were widowed and separated/divorced had reduced rates of co-infection, at 11.1% and 5.6% of co-infected patients, respectively. This agrees with previous findings (Okonko et al., 2020a).
The prevalence of HBsAg-HIV-1 co-infection was considerably higher in non-formal educational backgrounds (55.7%) than in other educational statuses. Also, the prevalence of Plasmodium falciparum-HIV-1 co-infection was considerably higher in the secondary educational background (26.0%) than in other educational statuses. Likewise, a higher prevalence of triple infections occurred among secondary (8.6%) and non-formal (8.5%) educational backgrounds compared to primary (6.2%) and tertiary (0.0%) educational backgrounds. The results of this investigation showed a complete divergence from those of the Okonko et al. (2023d,e) studies. This indicates that co-infection may be impacted by other factors, such as behavioural, socioeconomic, or environmental factors, and is not simply dependent on educational attainment. The intricacy of co-infections among HIV-1 patients in Bayelsa, Nigeria, is highlighted by these data overall. When developing intervention measures, healthcare professionals and policymakers must take into account the distinct demographics and traits of co-infected individuals. The fundamental causes of the observed gender- and education-related discrepancies in co-infection rates require more study to be better understood. Additionally, these results emphasize the significance. Surprisingly, the data showed that higher educational qualifications did not necessarily reduce the co-infection rate among patients.
This study indicated that occupation did not reduce the co-infection rate. The prevalence of HBsAg-HIV-1 co-infection was considerably higher among traders and those with undisclosed occupations (100.0%) than in other occupational statuses. Also, the prevalence of Plasmodium falciparum-HIV-1 co-infection was considerably higher in farmers (100.0%) than in other occupational statuses. Likewise, a higher prevalence occurred among those with undisclosed occupations (25.0%) compared to other occupational statuses with lower prevalence rates. This agrees with previous findings (Okonko et al., 2020a).
Overall, these findings underscore the complexity of co-infections among HIV-1 patients in Bayelsa, Nigeria. Healthcare providers and policymakers need to consider the unique demographics and characteristics of co-infected patients when designing intervention strategies. Further research is needed to better understand the underlying factors contributing to the observed gender and education-related disparities in co-infection rates. Additionally, these findings highlight the importance of integrated healthcare approaches that address multiple infections simultaneously, especially in regions where co-infections are prevalent.
The result also indicated that higher CD4 counts did reduce the co-infection rate. The prevalence of HBsAg-HIV-1 co-infection was considerably higher among those with CD4 counts ≤ 200 Cells/µl (50.0%) than in other categories. This observation conflicts with studies by Bhattarai et al. (2018) and Shrestha et al. (2022), which found that co-infection was less common in HIV patients with CD4 cells above 200 cells/mm3. Also, the prevalence of Plasmodium falciparum-HIV-1 co-infection was considerably higher in those with CD4 counts 200–349 Cells/µl (33.3%) than in other categories. Likewise, for HBsAg-Plasmodium falciparum co-infection, higher prevalence occurred in those with CD4 counts 200–349 Cells/µl (16.6%) compared to other categories with lower prevalence rates. This observation is not consistent with previous studies in Bayelsa (Okonko et al., 2023d,e) where higher triple infection of HIV/HBV/Plasmodium falciparum occurred in individuals with CD4 counts of above 500 Cells/µl.
A prospective observational cohort of adult patients with primary HIV infection has demonstrated that HBV coinfection was an independent predictor of immunologic progression, which was defined as the occurrence of a CD4 cell count of 350 cells/L 3 months or more after diagnosis of primary HIV infection. This reduces the impact of the duration of HIV infection. In a large cohort of HIV-infected people with a seroconversion window of 3 years, Chun et al. (2012) investigated the interactions of HBV and HIV using the composite endpoint of AIDS-defining illnesses and death. They found that the hazard ratio for an AIDS or death event was nearly double for those with HBV coinfection.
On the impact of HBV coinfection on HIV infection, Sun et al. (2014) stated that a persistent state of immune activation in patients with chronic HBV infection could up-regulate HIV replication, and an in vitro study showed that HBV X protein could induce ongoing HIV replication and long-term repeated transcription of HIV by synergizing with kappa B-like enhancer and T-cell activation signal. Early prospective cohort studies of HIV/HBV-coinfected patients revealed a 3.6 to 6.8-fold relative risk of progression to AIDS compared to those without coinfection. However, other reports failed to confirm these results. However, a CD4 count under 200 cells/µl still carries a substantial risk for opportunistic infections (Browne et al., 2000; Tay et al., 2015; Okonko et al., 2023d,e). According to George et al. (2015) and Wang et al. (2015), the declining CD4 cell count is a sign of HIV progression and immunological dysfunction, as well as co-infections and various opportunistic infections (Shrestha et al., 2022; Okonko et al., 2023d,e).
HBV and HIV co-infected individuals also have deteriorating liver disease, and HAART helps these patients. Additionally, co-infected patients with HBV and HIV experience worsening liver disease, and when these patients of receive HAART (highly aggressive anti-retroviral medication), their chance of developing liver disease increases even further. The study indicated that higher viral load did not follow any particular pattern in increasing the co-infection rate. The prevalence of HBsAg-HIV-1 co-infection was considerably higher among those with a viral load of ≤ 40 copies/ml (53.1%) and lower in those with 40-1000 copies/ml (44.1%) compared to those with ≥ 1000 copies/ml viral load (50.0%). This observation is consistent with previous studies in Bayelsa (Okonko et al., 2023d,e) where a higher coinfection rate occurred in individuals with a viral load of ≤ 40 copies/ml.
Also, the prevalence of Plasmodium falciparum-HIV-1 co-infection was considerably higher in those with a viral load of 40-1000 copies/ml (21.3%) compared to other categories. Likewise, a higher prevalence of HBsAg-Plasmodium falciparum co-infection occurred in those with a viral load of 40-1000 copies/ml (11.0%) compared to other categories with lower prevalence rates. This observation is not consistent with previous studies in Bayelsa (Okonko et al., 2023d,e) where higher triple infection of HIV/HBV/Plasmodium falciparum occurred in individuals with a viral load of 40-1000 copies/ml.
HIV and malaria each affect the other's transmission in regions where both diseases are endemic. Malaria causes an increase in HIV viral load, which raises the risk of HIV transmission and raises the prevalence of HIV. This could be the reason Sub-Saharan Africa also has the highest HIV prevalence. It has been hypothesized that HIV declines to extinction without the malaria-induced amplification effect. It has been suggested that a key element in the rapid spread of HIV infection in Sub-Saharan Africa is the recurrent transient elevations in HIV load caused by coinfection with malaria. Malaria's relative impact on HIV load may not be as significant. On the other hand, due to mechanisms involving immunosuppression, HIV infection raises the prevalence of Plasmodium falciparum parasitemia and is linked to severe malaria.
The presence of malaria and HBV co-infection has been known to influence the progression of either malaria, hepatitis, or both diseases. Nine per cent of hepatitis B virus (HBV) and malaria co-infections observed in this study show that they are endemic in most parts of Nigeria and Sub-Saharan Africa as seen in the study of Kolawole and Kana (2018) where co-infection of HBV and malaria accounted for 5.5% of their study population. Kolawole and Kana (2018) concluded that people with co-infections of HBV and malaria typically experience more alterations in their clinical states than people with mono-infections. In locations where HBV and malaria infections are co-endemic, there is a need for ongoing monitoring of people who come with febrile illnesses.
The impact of HIV and malaria co-infection is modified by such factors as the endemicity and stability of malaria transmission. It has been found that in areas with stable malaria transmission, HIV has been reported to increase the risk of malaria infection and clinical malaria in adults, especially those with advanced immunosuppression. Because natural immunity against malaria is not formed, leading to a high proportion of malaria cases, HIV-infected individuals are at higher risk of complicated and severe malaria fatalities in locations with unstable malaria transmission. This was demonstrated in a prospective study in South Africa by Cohen et al. (2005) where it was found that HIV-infected patients had a fourfold greater risk of developing severe malaria. Contrarily, research has revealed that malaria is significantly connected with HIV infection in eastern Sub-Saharan Africa but not in western Sub-Saharan Africa, indicating that malaria may not be a major factor in the spread of HIV in regions where the prevalence of the disease is low. More studies are required to confirm this.