PHINNOTY MWANSA

Dr. PHINNOTY MWANSA

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Research Focus & Metrics

Academic Career Length

2Years (2025-Present)

(Calculated once Scilit publication data is synced: current year − year of first publication + 1)

Representative Publications

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26 November 2025 in Biology
Verified
Journal Article
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David ChisompolaDavid Chisompola
David Chisompola
PMPHINNOTY MWANSA
PHINNOTY MWANSA
John NzobokelaJohn Nzobokela
John Nzobokela
MAMagdalene Ameka
Magdalene Ameka
Annet KiraboAnnet Kirabo
Annet Kirabo
Sepiso Kenias MasengaSepiso Kenias Masenga
Sepiso Kenias Masenga
HIV-induced apoptosis is a contradictory complicated phenomenon that occurs at the intersection of viral persistence and host defense. HIV primarily affects CD4 T cells during an infection, causing widespread immune cell death through both direct infection and indirect (bystander) mechanisms. This immunopathologic process is caused by viral proteins such as Tat, Nef, Env, and Vpr, which modify host signaling cascades such as the PI3K/Akt, p53, NF-κB, and mitochondrial pathways. Dysregulation of pro- and anti-apoptotic mediators, particularly Bax, Bcl-2, and caspase activation, which results in mitochondrial depolarization, oxidative stress, and cytochrome c release, exacerbates immune depletion. Although apoptosis serves as a host antiviral mechanism to limit viral replication and spread, HIV exploits it to evade immune surveillance and establish chronic infection. HIV pathogenesis, which includes lymphoid tissue destruction, microbial translocation, and persistent inflammation, is significantly influenced by apoptosis of both infected and bystander cells. Furthermore, alterations in death receptor signaling (Fas/FasL and TNF pathways) and mitochondrial dysfunction highlight the delicate balance between immune defense and viral manipulation. Despite considerable progress in antiretroviral therapy, immune restoration is still incomplete due to ongoing apoptotic loss and immune exhaustion. This review examines the biological mechanisms underlying HIV-induced apoptosis, evaluates the dual role of cell death in host defense versus viral persistence, and highlights novel therapeutic targets intended to restore immune homeostasis and reduce HIV-associated immunopathology.

6 April 2026 in PLOS ONE
Verified
Journal Article
Open access
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MMMwila Mapipo
Mwila Mapipo
AMAlex Maleti
Alex Maleti
PMPHINNOTY MWANSA
PHINNOTY MWANSA
PDPaul Daka
Paul Daka
David ChisompolaDavid Chisompola
David Chisompola
Introduction: Transfusion is a critical life-saving intervention, but the safety of the blood supply remains a major public health concern, particularly in sub-Saharan Africa, due to the risk of transfusion-transmitted infections (TTIs). This study aimed to determine the burden and correlates of bloodborne pathogens among blood donors in Muchinga Province, Zambia. Methods: A cross-sectional study was conducted using records from 2,667 blood donors at the Chinsali General Hospital Blood Bank between January and December 2021. Data on demographic characteristics, donation type, and ABO/Rhesus blood group were collected. Screening for Hepatitis B (HBV), Hepatitis C (HCV), HIV, and Syphilis was performed using the Abbott Alinity i platform. Logistic regression was used to identify factors associated with infection status. Results: The overall prevalence of TTIs among donors was 25.7% (686/2,667). The most prevalent single infections were HBV and Syphilis 8.0% (213/2,667), followed by HCV 7.8% (207/2,667), and HIV 7.7% (206/2,667), with notable co-infection rates, particularly HIV/Syphilis (4.9%). In the composite multivariable analysis, donors with blood group O had 36% lower adjusted odds of any TTI compared to those with blood group A (AOR = 0.64; 95% CI: 0.52–0.79; p < 0.0001) and individuals aged over 45 years had 45% higher adjusted odds of TTIs compared to those aged 16–24 years (AOR = 1.45; 95% CI: 1.04–2.00; p = 0.026). Furthermore, multivariable pathogen-specific analyses revealed distinct risk profiles: donors aged ≥45 years had significantly higher odds of syphilis (AOR = 2.38; 95% CI: 1.49–3.80; p < 0.0001), female sex was associated with lower odds of HBV (AOR = 0.69; 95% CI: 0.52–0.93; p = 0.016), blood group O was protective against HCV (AOR = 0.49; 95% CI: 0.35–0.69; p < 0.0001), and donors from Mpika district had higher odds of HIV (AOR = 1.82; 95% CI: 1.03–3.21; p = 0.037). Conclusion: This study highlights a substantial burden of TTIs among blood donors and identifies blood group O as a potential protective factor, suggesting a potential biological basis that requires further study. Strengthened donor screening and public health interventions are critical to improving blood safety.

12 August 2026 in Discover Public Health
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Journal Article
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PMPHINNOTY MWANSA
PHINNOTY MWANSA
DCDavid Chisompola
David Chisompola
SMStella P. Mainga
Stella P. Mainga
JPJoreen P. Povia
Joreen P. Povia
Sepiso Kenias MasengaSepiso Kenias Masenga
Sepiso Kenias Masenga
Immunoglobulin E (IgE) is traditionally recognized for its role in allergic response. However, emerging evidence suggests it may also influence cardiovascu

12 May 2026 in PLOS Global Public Health
Verified
Journal Article
Open access
SMSydney Mulamfu
Sydney Mulamfu
David ChisompolaDavid Chisompola
David Chisompola
MCMartin Chakulya
Martin Chakulya
JNJohn Nzobokela
John Nzobokela
PMPHINNOTY MWANSA
PHINNOTY MWANSA
Sepiso Kenias MasengaSepiso Kenias Masenga
Sepiso Kenias Masenga
Left ventricular hypertrophy (LVH) is a significant cardiovascular complication in sub-Saharan Africa. However, sex-specific determinants of LVH in this population remain poorly understood. This study aimed to identify factors associated with LVH in a cohort attending medical clinic, stratified by sex. We conducted a cross-sectional analysis of 333 adults attending an outpatient clinic at Livingstone Teaching Hospital, Zambia. LVH was diagnosed by echocardiography. Data on demographics, clinical history (HIV, TB, hypertension) and metabolic profiles were collected. Univariable and multivariable logistic regression models were used to identify predictors of LVH in the overall cohort and in sex-stratified subgroups. p < 0.05 was considered statistically significant. Data from 333 participants were analysed. LVH was diagnosed in 75 participants (22.5%). In the overall cohort, independent factors associated with LVH were older age (AOR: 1.06 per year, 95% CI: 1.03–1.09, p < 0.0001), female sex (AOR: 2.31, 95% CI: 1.13–4.68, p = 0.020), hypertension (AOR: 2.52, 95% CI: 1.36–4.66, p = 0.003), and heart failure (AOR: 7.50, 95% CI: 1.85–30.3, p = 0.005). Sex-stratified analysis revealed distinct profiles: in males, LVH was significantly associated with older age (AOR: 1.06, 95% CI: 1.00–1.13, p = 0.030), hypertension (AOR: 3.70, 95% CI: 1.03–13.2, p = 0.044), and heart failure (AOR: 18.3, 95% CI: 1.60–209.0, p = 0.019), whereas in females, factors associated with LVH included older age (AOR: 1.06, 95% CI: 1.03–1.09, p < 0.0001), hypertension (AOR: 2.50, 95% CI: 1.21–5.18, p = 0.013), waist circumference (AOR: 1.05 per cm, 95% CI: 1.00–1.10, p = 0.047), and elevated cholesterol-HDL ratio (AOR: 1.53, 95% CI: 1.02–2.30, p = 0.036). LVH in this cohort was associated with age, female sex, hypertension, and heart failure. Factors associated with LVH differed by sex, with metabolic factors playing a more prominent role in women and hemodynamic factors in men. These findings underscore the importance of sex-specific cardiovascular risk assessment and tailored management strategies.