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 International Journal of Medical Sciences and Pharma Research 

Open Access to Medical Science and Pharma Research

Copyright  © 2025 The   Author(s): This is an open-access article distributed under the terms of the CC BY-NC 4.0 which permits unrestricted use, distribution, and reproduction in any medium for non-commercial use provided the original author and source are credited

 

Risk of Opportunistic Infections in Sickle Cell Patients with HIV: A Review

Emmanuel Ifeanyi Obeagu ¹* and Priya Homa Chukwu ²

¹ Department of Biomedical and Laboratory Science, Africa University, Zimbabwe

² Department of Haematology and Blood Transfusion Science, Faculty of Medical Laboratory Science, Rivers State University of Science and Technology, Port Harcourt, Rivers State, Nigeria

 

 

Introduction

Sickle cell disease (SCD) and human immunodeficiency virus (HIV) are two chronic conditions that independently compromise the immune system. SCD is an inherited hematologic disorder characterized by the production of abnormal hemoglobin S, leading to chronic hemolysis, vaso-occlusion, and progressive organ damage. HIV, on the other hand, is an acquired immunodeficiency that weakens the immune system by depleting CD4+ T cells, increasing susceptibility to opportunistic infections (OIs). The co-existence of these two conditions poses significant challenges in clinical management due to the compounded effects of immune dysfunction.^1-2 The immune system in SCD patients is compromised due to functional asplenia, chronic inflammation, and impaired phagocytic function. This leads to an increased risk of infections caused by encapsulated bacteria such as Streptococcus pneumoniae and Haemophilus influenzae. In HIV, immune suppression results in a broader susceptibility to bacterial, fungal, viral, and parasitic infections. The combined impact of these immune alterations in co-infected individuals results in a higher burden of severe infections compared to patients with either condition alone.^3-4 Several studies have suggested that SCD-related immune dysfunction may accelerate the progression of HIV and increase the severity of opportunistic infections. Chronic hemolysis and inflammation in SCD can further activate the immune system, potentially worsening HIV-induced immune exhaustion. Additionally, recurrent infections and chronic anemia in SCD may complicate the effectiveness of antiretroviral therapy (ART), leading to suboptimal treatment outcomes.^5-6

Opportunistic infections in SCD-HIV co-infected patients are diverse and often more severe due to overlapping immune deficits. Bacterial infections, including tuberculosis and pneumococcal infections, are more frequent and severe in this population. Fungal infections such as cryptococcal meningitis and candidiasis also present significant risks. Moreover, viral infections like cytomegalovirus (CMV) and parvovirus B19 can lead to severe complications, including life-threatening anemia. Parasitic infections such as malaria and toxoplasmosis further contribute to morbidity and mortality in these patients.^7-8 The prevention and management of opportunistic infections in SCD-HIV co-infected individuals require a multifaceted approach. Vaccination against pneumococcus, meningococcus, influenza, and hepatitis B is essential in reducing infection risks. Antimicrobial prophylaxis with cotrimoxazole and penicillin is also recommended to prevent bacterial infections. Early initiation of ART is critical in preserving immune function, though careful selection of drugs is necessary to avoid hematologic toxicity and drug interactions with SCD treatments.^9-10

Immunological Basis for Increased Susceptibility

The immune dysfunction observed in sickle cell disease (SCD) and human immunodeficiency virus (HIV) co-infection results from a combination of factors, including impaired splenic function, chronic inflammation, and progressive immunosuppression. While SCD leads to functional asplenia and abnormal immune cell function, HIV exacerbates immune dysregulation by targeting CD4+ T cells and impairing both innate and adaptive immunity. These overlapping mechanisms significantly increase the risk of opportunistic infections (OIs) in co-infected individuals.^11-12

Sickle Cell Disease-Induced Immune Dysfunction

SCD is characterized by chronic hemolysis, inflammation, and oxidative stress, all of which contribute to immune dysregulation. One of the most significant immunological impairments in SCD is functional asplenia, where repeated splenic infarctions reduce or eliminate the spleen's ability to filter pathogens. This renders individuals highly susceptible to infections caused by encapsulated bacteria such as Streptococcus pneumoniae, Haemophilus influenzae, and Neisseria meningitidis. Additionally, SCD patients exhibit abnormal neutrophil and monocyte function, leading to impaired pathogen clearance.^13-14 Chronic inflammation in SCD results from ongoing hemolysis and vaso-occlusion, which lead to the persistent activation of immune cells, including neutrophils, monocytes, and macrophages. This hyperactivation contributes to immune exhaustion, reducing the ability to mount an effective response to infections. Furthermore, complement system dysfunction has been reported in SCD patients, further impairing the body's ability to clear pathogens efficiently. These immune alterations make SCD patients particularly vulnerable to bacterial and fungal infections.^15-16

HIV-Associated Immunosuppression

HIV primarily targets CD4+ T cells, leading to progressive immune system depletion. The loss of these critical immune cells impairs adaptive immunity, making it difficult to control infections. HIV also disrupts antigen-presenting cell function, further compromising the ability to generate an effective immune response. As a result, individuals with HIV are highly susceptible to opportunistic infections, including tuberculosis, pneumocystis pneumonia, cryptococcosis, and viral reactivations such as cytomegalovirus (CMV) and Epstein-Barr virus (EBV).^17-18 Additionally, chronic immune activation in HIV infection contributes to systemic inflammation and immune exhaustion. The continuous stimulation of immune cells leads to the overproduction of pro-inflammatory cytokines, such as tumor necrosis factor-alpha (TNF-α) and interleukin-6 (IL-6), which further impair immune function. This persistent inflammatory state is worsened by the underlying chronic inflammation in SCD, creating a cycle of immune dysregulation that increases susceptibility to infections.^19-20

Impact of Dual Immune Dysregulation on Opportunistic Infections

The combination of SCD-induced immune impairments and HIV-mediated immunosuppression leads to an exceptionally high risk of OIs in co-infected individuals. The inability to effectively clear bacterial pathogens due to asplenia and neutrophil dysfunction is compounded by HIV-induced defects in adaptive immunity. Similarly, fungal and viral infections that are already prevalent in HIV patients may become even more severe in individuals with SCD due to the additional burden of chronic inflammation and oxidative stress.^21-22 Furthermore, the dysregulation of cytokine networks in both conditions contributes to a paradoxical immune response, where persistent inflammation coexists with immune suppression. This immune imbalance not only increases infection susceptibility but also exacerbates disease progression and complications in both SCD and HIV. As a result, co-infected individuals experience higher morbidity and mortality rates compared to those with either condition alone.^23-24

Common Opportunistic Infections in SCD-HIV Co-Infected Patients

Individuals with both sickle cell disease (SCD) and human immunodeficiency virus (HIV) are at an increased risk of opportunistic infections (OIs) due to their compromised immune systems. SCD-related functional asplenia and chronic inflammation weaken the body’s ability to clear pathogens, while HIV further suppresses immune function through CD4+ T-cell depletion. This dual immunosuppression makes co-infected individuals highly vulnerable to a range of bacterial, fungal, viral, and parasitic infections.^25-26

Bacterial Infections

Bacterial infections are among the most frequent and severe OIs in SCD-HIV co-infected patients. Due to functional asplenia, individuals with SCD have a diminished ability to clear encapsulated bacteria, while HIV-induced immunosuppression exacerbates this vulnerability.

• Streptococcus pneumoniae and Haemophilus influenzae: These encapsulated bacteria cause severe respiratory and systemic infections, including pneumonia, meningitis, and sepsis. The risk of invasive pneumococcal disease is significantly elevated in SCD patients and worsened by HIV-related immune suppression.^26-27
• Mycobacterium tuberculosis: Tuberculosis (TB) is a major concern in HIV patients and is further aggravated in individuals with SCD due to chronic inflammation and lung damage caused by repeated vaso-occlusive episodes. TB in co-infected patients often presents with severe or disseminated forms, requiring aggressive management.²⁸
• Salmonella species: SCD patients have a higher susceptibility to Salmonella infections, leading to osteomyelitis and bacteremia. In HIV patients, Salmonella infections tend to be more invasive and recurrent, contributing to increased morbidity.²⁹

Fungal Infections

Fungal infections in SCD-HIV co-infected patients can be life-threatening, particularly in those with advanced immunosuppression.

• Cryptococcus neoformans: Cryptococcal meningitis is a leading cause of morbidity and mortality in HIV-infected individuals, and co-infection with SCD increases the risk of severe neurological complications.³⁰
• Candida species: Oral and esophageal candidiasis are common in HIV patients, and individuals with SCD may experience prolonged or more severe infections due to immune dysregulation.³¹
• Histoplasma capsulatum: Histoplasmosis, a fungal infection endemic in certain regions, can cause disseminated disease in HIV-infected patients. SCD-related immune dysfunction may contribute to more aggressive disease progression.³²

Viral Infections

HIV increases susceptibility to viral infections, many of which can lead to serious complications in patients with SCD.

• Cytomegalovirus (CMV): CMV infection is common in HIV patients with low CD4+ counts, causing complications such as retinitis, colitis, and pneumonia. The added stress of SCD-related inflammation may worsen disease severity.³³
• Parvovirus B19: Parvovirus B19 infection can cause aplastic crisis in SCD patients by suppressing erythropoiesis, leading to life-threatening anemia. In HIV-infected individuals, chronic parvovirus infection can result in persistent anemia and bone marrow failure.³⁴
• Epstein-Barr Virus (EBV): EBV infection is associated with an increased risk of malignancies such as Burkitt’s lymphoma in immunocompromised individuals. SCD patients, who may already have a predisposition to hematological complications, are particularly vulnerable.³⁵

Parasitic Infections

Parasitic infections remain a significant concern, especially in regions where malaria and other parasitic diseases are endemic.

• Plasmodium falciparum (Malaria): Although individuals with SCD have some genetic protection against severe malaria, HIV co-infection weakens this advantage, increasing the risk of severe malaria-related complications such as cerebral malaria and multi-organ failure.³⁶
• Toxoplasma gondii: Toxoplasmosis is a serious OI in HIV patients, leading to encephalitis and neurological dysfunction. SCD-related anemia and immune dysregulation can worsen disease outcomes.³⁷
• Strongyloides stercoralis: Chronic strongyloidiasis, a parasitic infection affecting the gastrointestinal tract, can become disseminated in immunocompromised individuals, causing severe complications.³⁸

Impact of Opportunistic Infections on Disease Progression

OIs contribute significantly to morbidity and mortality in SCD-HIV co-infected patients. The combination of frequent infections, chronic inflammation, and immune exhaustion accelerates disease progression and increases hospitalization rates. Many of these infections lead to severe complications, such as multi-organ dysfunction, neurological impairments, and life-threatening anemia. Therefore, early detection, prophylaxis, and appropriate treatment strategies are critical in improving survival and quality of life in affected individuals.³⁹

Prevention and Management Strategies

Managing opportunistic infections in sickle cell disease (SCD) patients co-infected with human immunodeficiency virus (HIV) requires a multifaceted approach that addresses both immune dysfunction and the heightened susceptibility to infections. Given the overlapping immunological challenges of these two conditions, prevention strategies such as vaccination, antimicrobial prophylaxis, and early antiretroviral therapy (ART) initiation plays a crucial role in reducing infection-related morbidity and mortality. Additionally, optimizing the management of SCD through hydroxyurea therapy, regular transfusions, and supportive care can help strengthen immune defenses and prevent severe complications.⁴⁰ Vaccination remains one of the most effective preventive measures in SCD-HIV co-infected individuals. Since SCD patients experience functional asplenia and HIV patients have compromised immune responses, both groups are at an increased risk of bacterial infections, particularly from Streptococcus pneumoniae, Haemophilus influenzae, and Neisseria meningitidis. Pneumococcal conjugate and polysaccharide vaccines, along with the Haemophilus influenzae type B (Hib) and meningococcal vaccines, are essential in reducing the risk of life-threatening infections. Annual influenza vaccination is also recommended to prevent respiratory complications, which can be particularly severe in SCD patients who already face the risk of acute chest syndrome. Hepatitis B vaccination is another important preventive measure, especially for HIV-infected individuals who may be more susceptible to co-infections due to frequent blood transfusions.⁴¹

In addition to vaccination, antimicrobial prophylaxis plays a critical role in infection prevention. Long-term penicillin prophylaxis is commonly recommended for SCD patients, particularly in early childhood, to protect against pneumococcal infections. Meanwhile, cotrimoxazole prophylaxis is a key intervention in HIV care, preventing Pneumocystis jirovecii pneumonia (PJP) and reducing the risk of bacterial infections. For individuals living in malaria-endemic regions, antimalarial prophylaxis is necessary, as SCD patients are highly susceptible to severe malaria, which can exacerbate anemia and lead to fatal complications. Furthermore, in cases of advanced immunosuppression, antifungal prophylaxis may be considered to prevent opportunistic fungal infections, particularly cryptococcosis.⁴² Early initiation and careful selection of ART are crucial for improving immune function in SCD-HIV co-infected individuals. While ART helps suppress viral replication and reduce HIV-related immunosuppression, some regimens may pose additional risks due to hematologic side effects. For instance, zidovudine (AZT) is often avoided in SCD patients due to its potential to worsen anemia. Instead, alternative nucleoside reverse transcriptase inhibitors (NRTIs) such as tenofovir disoproxil fumarate (TDF) or abacavir (ABC) are preferred. Additionally, potential interactions between ART and hydroxyurea—an essential therapy for reducing vaso-occlusive crises in SCD—must be carefully monitored to ensure efficacy and minimize toxicity. Adherence counseling is also essential, as managing both SCD and HIV requires a complex regimen of medications that can be challenging for patients.⁴³

Optimizing SCD management is another key aspect of reducing infection risk. Hydroxyurea therapy, which increases fetal hemoglobin levels and reduces sickling episodes, has been shown to lower inflammation and improve overall immune function in SCD patients. Regular blood transfusions are also used to manage severe anemia and prevent complications such as stroke. However, transfusions must be administered cautiously in HIV-infected patients due to the risk of iron overload, alloimmunization, and potential transmission of transfusion-related infections. Effective pain management, hydration, and oxygen therapy are critical in preventing vaso-occlusive crises, which can lead to prolonged hospitalizations and an increased risk of secondary infections.^44-45 Routine screening and early detection of opportunistic infections are fundamental in preventing severe complications. Regular tuberculosis (TB) screening using tuberculin skin tests or interferon-gamma release assays (IGRAs) is necessary in co-infected patients, as they are at a higher risk of TB reactivation. Blood and urine cultures should also be performed in cases of unexplained fever or suspected sepsis to ensure early and appropriate antibiotic therapy. Additionally, testing for cytomegalovirus (CMV) and parvovirus B19 is important, particularly in HIV-infected patients with persistent anemia or fever.^46-47 Nutritional and supportive care further contributes to strengthening immune function and reducing infection risk. Addressing micronutrient deficiencies, such as vitamin D, zinc, and folate, can enhance immune resilience and reduce inflammation. Psychosocial support, patient education, and mental health counseling are equally important, as the burden of managing both SCD and HIV can significantly impact emotional well-being and treatment adherence.⁴⁸

Conclusion

Sickle cell disease (SCD) and human immunodeficiency virus (HIV) co-infection present a significant clinical challenge due to the compounded effects of immune dysfunction, chronic inflammation, and increased susceptibility to opportunistic infections (OIs). The combination of SCD-related functional asplenia and HIV-induced immunosuppression leaves affected individuals highly vulnerable to bacterial, fungal, viral, and parasitic infections, which contribute to increased morbidity and mortality. These infections, if not adequately managed, can lead to severe complications, prolonged hospitalizations, and poor disease outcomes. Prevention and management strategies must be comprehensive and tailored to the unique needs of SCD-HIV co-infected patients. Vaccination, antimicrobial prophylaxis, and early initiation of antiretroviral therapy (ART) play a crucial role in reducing the incidence of OIs. Additionally, optimizing SCD management through hydroxyurea therapy, regular transfusions, and supportive care can help improve immune function and reduce complications. Routine screening for infections, coupled with prompt and effective treatment, is essential in mitigating the impact of OIs.

Conflict of Interest: Author declares no potential conflict of interest with respect to the contents, authorship, and/or publication of this article.

Source of Support: Nil

Funding: The authors declared that this study has received no financial support.

Informed Consent Statement: Not applicable. 

Data Availability Statement: The data supporting in this paper are available in the cited references. 

Ethics approval: Not applicable.

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