Preprint
Review

This version is not peer-reviewed.

Hazardous Clinical Conditions Present Specific Transfusion-Transmitted Disorder Risks and Require Special Attention: Sickle Cell Disease, Transplantation Settings

Submitted:

10 September 2025

Posted:

11 September 2025

You are already at the latest version

Abstract
Aims: The aim is to focus on the risk of transfusion-transmitted diseases, which are emerging in highly vulnerable conditions, especially in hazardous disorders such as sickle cell disease, specific clinical situations, and transplantations. Transplant settings require even greater vigilance in donor selection, blood preparation, and pathogen screening. They may also involve new lifestyle considerations for the safe selection of organ or stem cell donors—a deeper consideration is essential regarding the hepatitis E virus and vidarabine resistance in these high-risk patient groups. Clinical settings: This brief review emphasises a high-risk group of patient cohorts for bloodborne infections, their transfusion needs, and the criteria for transfusion. The most significant topic is arguably a complex and severe haemoglobinopathy, sickle cell disease (SCD), which requires frequent transfusions for critically important reasons, particularly because sickling prevention, splenic function, and in the meanwhile immune defence are often impaired. Some pathogens, such as parvovirus B19, pose particular risks in SCD. Bone marrow and solid organ transplantation as potential transmission routes during and after the procedure will also be examined, emphasising more recent data across various transplant scenarios.
Keywords: 
;  ;  ;  ;  ;  

Introduction

This brief review will highlight a specifically endangered genetic haemoglobinopathy, namely Sickle Cell Disease (SCD). It is arguably the most serious and complex congenital haemoglobin abnormality. From a clinical perspective, it is characterised by numerous sickled red blood cell clumps, provoked vaso-occlusive signs and crises, along with haematological abnormalities that often require frequent transfusions. In most cases, these conditions are also associated with hypo-asplenic states. This combination necessitates extra efforts to prevent transfusion-transmitted disorders, especially in multitransfused patients with poorly functioning spleens and compromised immune defences. Sickling may be significantly reduced by innovative therapies, mainly based on cell modifications, which will be briefly discussed. However, these approaches may also pose risks of pathogen transmission. Additionally, new data on the Hepatitis E virus in vulnerable patients is presented, with a particular focus on the vidarabine-refractory case therapy after transplants. Updated information on transmissible diseases in bone marrow and organ transplant recipients is also included, whether donor- or transfusion-derived.

A. Sickle Cell Disease (SCD)

The importance of sickle cell disease (SCD) is often underestimated. It is not limited to sub-Saharan Africa and African Americans but also affects Hispanic communities, as well as a large number of individuals in India, the Middle East, and even in Greece. The number of SCD cases is increasing [1,2,3]. Most cases still occur in sub-Saharan countries, such as Nigeria and the Democratic Republic of the Congo, with a 70% rise in reported cases over the past decade. Undoubtedly, African American populations (approximately 8 million homozygous patients and over 300,000 deaths annually) continue to represent a larger share, living within a healthcare system that is better resourced. However, this also impacts Hispanic communities across the United States, the Caribbean, Brazil, Colombia, and other regions. A growing number of cases are being observed in several Middle Eastern countries. Some cases (0.2-2.7%) have been identified even in Greece, and it is clear that a substantial cohort of patients exists in India as well. The percentage of homozygous cases is similar to that seen in North America, but the population is much larger. Additionally, medical standards vary more widely.
Therefore, a brief overview of the clinical course is necessary, emphasising the critical role of red cell transfusion in patients with hypo- and asplenic conditions. Issues related to bloodborne diseases are of particular concern, particularly regarding infections (such as parvovirus B19 and hepatitis C) or the development of vascular events and bone marrow aplasia [4,5,6,7].
The beta-globin gene on chromosome 11 has experienced a mutation, leading to the production of HbS. This severe condition endangers individuals with homozygous cases, while those with heterozygous cases (sickle cell trait) usually have minimal symptoms. The oxygen-carrying capacity of the mutated haemoglobin in HbS is decreased (similar to other thalassaemias). Additionally, red blood cells containing HbS often change shape and can become sickle-shaped (sickling). These sickled cells are too rigid for proper circulation in the microvasculature. Various vaso-occlusive crises may occur when sickling increases (sometimes due to known background, though others are due to not yet fully understood provocative factors). These crises can cause acute pain, stroke, coronary occlusion (even in infants as young as 6 months), and chronic organ damage [7,8,9,10,11].
The survival data for SCD homozygous African Americans is limited; their expected lifespan is relatively low. It is 20-25 years shorter than that of other African Americans. The two main traditional elements of vaso-occlusive event prevention are based on strategies for reducing the proportion of HbS in the blood, by giving RBC transfusions frequently. These are systemic, repeated courses of hydroxyurea along with frequent, repeated transfusions, and of course protecting antimicrobial immunity or administering such agents [2,5,11,12].
However, some types of innovative, more recent therapy show real promise in terms of lifespan improvement. These include allogeneic transplantation, P-selectin inhibition to block vaso-occlusive events (crisanlisumab) and, most importantly, gene modification of the red blood cells of SCD patients. This achieves better oxygen affinity and avoids sickling, as demonstrated by Lyfgenia and Casgevy [13,14].
These measures may prolong survival and, in the meantime, facilitate an increase in infections, including transfusion-transmitted infections, among polytransfused patients. Still, they may also carry a small risk of pathogen transmission through cell therapy.

Transfusion-Transmitted Disorders in SCD

As previously noted, the social background, haemovigilance, and preparatory measures for blood transfusion in SCD patients vary considerably across different regions. The transmission of the classical quartet (HBV, HCV, HTLV-1, and HIV) was widespread 20-25 years ago. HCV remains a significant concern, with high rates (ranging from 40-60%) still present in less-developed countries. Improvements in blood preparation safety have led to a notable reduction in the incidence of HTLV and HBV, with an approximate 2% decrease observed in most countries involved. However, HCV continues to be an issue. In SCD patients who have undergone numerous transfusions (10 or more), prevalence rates of up to 12% or higher have been reported, indicating a complex underlying cause. This includes differences in molecular virus detection levels and genotype shifts of the C virus [15,16,17,18].
Patients with SCD who have received more than 10 transfusions seem particularly vulnerable to parvovirus B19 transmission, regardless of the route of infection. In cases of pure red cell aplasia in SCD, where the condition is usually rapid and severe, and rarely treatable or curable, Parvo B19 can also trigger acute vaso-occlusive events. This is a serious condition and, even more concerning, can lead to an acute aplastic bone marrow crisis, involving the destruction of all precursor cell lines. Similar to severe aplastic anaemia. This condition can be fatal and develops quickly. In some cases, treatments such as intravenous immunoglobulins and anti-CD38 monoclonal infusions are not quick enough. Although mortality remains high, treatments such as transfusions, supportive therapies, and Rescue of allogeneic bone marrow transplants might be considered.
Chronic hepatitis B virus (HBV) infection is common among patients with sickle cell disease (SCD), as shown by extensive studies from the United States, with seropositivity for HBsAg ranging from 0 to 3.3 percent. In regions where HBV is more widespread, higher rates of chronic HBV have been observed in patients with SCD compared to the general population. The hepatitis C virus (HCV) has been detected in 10 to 20 percent of patients with SCD [19]. Patients who have received multiple transfusions are at greater risk of infection. In one particular study, the presence of antibodies to HCV was identified more frequently among patients who had received more than 10 units of packed red blood cells (23% versus 8% and 0% in those who had received fewer than 10 units or no transfusions, respectively). Thanks to improved screening techniques, the risk of acquiring HCV through blood transfusions in the US has become very low (about 1 in 1,900,000). In Egypt, twenty-three per cent of patients (16 individuals) tested positive for HCV antibodies; 56.3% of these (9 individuals) had undetectable HCV RNA in their serum, and 43.7% (7 individuals) had persistent viremia.
Hepatitis C virus leads to serious consequences in SCD, including chronic liver disease, increased risk of complications and higher rates of liver cancer compared to non-SCD patients [17,18,19].
The C virus genotypes CC/CT/TT of rs12979860 were detected in 30 (42.9%), 29 (41.4%), and 11 (15.7%) patients, while the rs12980275 AA/AG/GG genotypes were found in 8 (11.4%), 59 (84.3%), and 3 (4.3%) patients. No significant difference was observed in the frequency of IL28B (rs12979860 and rs12980275) genotypes among HCV patients who cleared the virus and those with persistent viremia (p = 0.308 and 0.724, respectively). Egyptian SCD patients show a high prevalence of HCV; multi-transfused patients remain at risk of HCV transmission. In this group of Egyptian children with SCD, IL28B gene polymorphisms are not linked to spontaneous HCV clearance. HCV IL28B polymorphism is associated with improved HCV clearance [19]. HCV vaccination effort in China might be considered extremely important; however, the vaccine is not commercially available yet.
SCD patients should be prepared for more severe acute hepatitis symptoms, primarily due to chronic Liver iron overload, likely accompanied by bilirubin-type gallstones and secondary cholecystitis. The presence of extrahepatic manifestations (e.g. proteinuria, cytopenia, neurological signs) is more common and requires specialised care.

Blood Group Alloimmunity in SCD

The clinical observations suggest that the best anti-infection defence is in individuals with blood Group 0+. Although bacterial infections are uncommon, they account for 16% of transfusion-related fatalities. Patients who are iron overloaded like SCD) are particularly susceptible to Yersinia enterocolitica. Red cell alloimmunisation is a serious issue that could potentially affect 50% of transfused patients. However, preventive phenotypic matching for common antigens can reduce alloimmunisation; limited matching for at least E, C, and K has become the standard of care.
Some parallels can be drawn between blood group alloimmunisation and other non-SCD polytransfused cases. In this context, Rh issues are critically important because, unlike in different clinical settings, hemolysis can be more severe and lead to vaso-occlusive episodes. Furthermore, the presence of Rh-specific alloimmunisation can be detected in 5-41% of cases. Simple matching revealed alloimmunisation in 0-5% of cases, while extended matching showed a rate of 0-24%. This is much higher than in other patients who have received multiple transfusions. In SCD, immunosuppression appears to be particularly risky, and reducing leukocytes might be a beneficial strategy [20,21]. Packed red cells are the preferred blood component. Leukocyte-reduced units should be standard due to their beneficial effects in reducing alloimmunisation, transfusion reactions, platelet refractoriness, and the transmission of infections.
Blood group alloantigen positive patients may have impaired immunological defence, some encapsulated, COVID-19, or sometimes Parvo B19 might develop

B. More Recent Data on the Hepatitis E Virus (HEV)

Approximately 12% of the general population in various countries are HEV IgG positive, and most cases probably remain undetected in Africa. There are eight different genotypes of HEV. The most common phenotypes include HEV 1-4. In Latin America, Africa, and Asia, HEV 1 and 2 are the most prevalent, with the latter two being transmitted through contaminated drinking water. Many mammals are susceptible to infection by HEV 3 and 4, which can be transmitted through contact with undercooked food or via the faecal route [22]. These major HEV genetic variants have further subtypes with different properties. They can react to interferons of types I, II, and III, and they can exhibit antiviral actions during both the acute and chronic phases. The interferon response can be impaired in immunosuppressed patients [22,23,24,25].
The hepatitis E genotype is essential in two specific contexts: SCD and certain transplant settings. The 205 participants with SCD in the survey included 115 males (56.1%) and 90 females (43.9%). Two or more transfusions were received by 99 (48.8%) of the patients, while 49 (23.9%) had received only one. 57 (27.8%) participants had never had a transfusion. Patients receiving anti-CD20 therapies are at a higher risk of acquiring HEV [24,25].
Increasingly, whole-genome sequencing is used to study HEV, and some variants and mutants have been identified as resistant to standard anti-HEV treatments, such as ribavirin. These are sometimes sequence snippets or insertions in the large HEV hypervariable region. (WU). A survey of kidney transplant recipients from Japan revealed that HEV anti-IgG was present in 4.3% of the study participants, while IgM positivity was absent. The results were consistent across all patients. Patients with HEV IgG were slightly older and had received more transfusions before transplant. HEV serology is likely essential in this setting [25].
PEG interferon might be introduced if ribavirin proves ineffective. HEV vaccination—approved in China but not yet available—may also be necessary. Sobosovir combined with ribavirin is a promising option. However, HEV genetic variants A1343V and G1364R, whether alone or combined, may also develop resistance to Sobosovir. These genetic alterations could be part of a response to treatment, even if they are present from the beginning [24,25].
In some instances, vidarabine-based antiviral treatment necessitates prolonged durations. During relapse, the therapy’s efficacy diminishes; whereas healthy populations show a 90 per cent response rate, SCD and post-transplant cases only attain a positive response of around 40 per cent [26,27,28,29].

Organ Transplants

The donor’s pre-transplant examination and infection screening are essential whenever a living donor method is used. In cases of brain-death but heart-beating donors, the screening period is limited due to the short cold-reperfusion time caused by biological factors, and at he same time they remain in intensive care units loaded with potential iatrogenic pathogens. If there is an urgent need to transplant a cadaver organ, the cold-reperfusion period is even briefer, which prevents sufficient time for thorough HLA and pathogen testing. In such situations, it is even more essential to focus on lifestyle factors and consider the threats common to the geographical region and its surrounding areas. Screening of living donors is becoming increasingly important across all transplantation scenarios. Dogs and raccoons (mainly dogs in China) should be screened for active tuberculosis [29,30].
Donor screening is already complicated enough, but it could become even more so due to unexpected transmissible diseases and certain lifestyle factors (such as rafting, rock climbing, and close contact with some animals) [30,31,32].
Trypanosoma cruzi, Strongyloides stercoralis, West Nile virus, Brucella, and rabies, especially if there has been close contact with dogs. In Spain, cases of organ transplant transmission of Leishmania have been reported. Leptospira, along with activities such as agricultural work, rafting, and rock climbing, have also been linked to a silent infection which might be transmissible. Travelling to regions with a high risk of malaria, leishmaniasis, schistosomiasis, or strongyloidiasis increases the risk of infection in patients who have undergone a transplant (bone marrow or organ, depending on the type and level of immunosuppression) [33,34,35]. Toxoplasmosis is one of the most significant concerns in Europe, especially in heart and bone marrow transplants (including haploidentical cases). Disseminated cases are often associated with high mortality. Therefore, caution is vital, and transplant teams must remain vigilant. It is also important to note that low-level oncogenic hepatitis B virus variants can persist despite effective anti-HBV prophylaxis in some organ transplant recipients [33,34].
Torque teno (TT virus), a potential pathogen, is detected more often in cases of chronic haemodialysis (17%) and kidney transplant (36%). The TT virus genotype varies, but the clinical courses remain similar. Further studies and close monitoring are needed to understand the clinical significance of this phenomenon [36,37]. Kidney transplant patients, especially those without HLA-A2, are more prone to immune responses against organs from CMV-positive donors due to the virus. These responses are characterised by T cells that produce IFN-γ and are specific to the virus. Most of these cases have silent clinical courses, but CMV screening should be carefully considered in organ transplants, depending on the recipient’s CMV status and the potential for reactivation [35,36,37,38].
It is interesting to note that even a cornea transplant, where blood flow is limited, cannot be considered entirely free from transmission, despite the extremely low likelihood of this occurring. Two cases of HBV and two cases of Creutzfeldt-Jakob disease have been documented. Contact lenses worn by the donor can increase the chance of transmitting these diseases and, interestingly, also contribute to the development of neurological and cognitive disorders. It may be advisable not to use corneal tissue from patients who have previously worn contact lenses [39].
There is an increasing amount of data on organ and stem cell transplants (as well as other types of cell therapies) and blood-borne infections. These cases, such as arboviruses like dengue, chikungunya, tick-borne encephalitis, WNV, and Zika virus, are transmitted from animals to humans. HEV is a zoonosis, meaning it can cause more severe liver and other health issues, and it can reduce the effectiveness of antiviral treatments, particularly in organ transplant patients. Lymphocytic choriomeningitis and ehrlichiosis should also be considered [35,37,38,39].

Bone Marrow Transplantation

Of course, standard viral screening, bacterial, and other pathogen examinations are critical in bone marrow donors; the procedure allows sufficient time for this. The CMV status of the donor and patient is highly significant [40,41,42,43], even though opinions may not be entirely consistent and vary. Parvovirus B19 screening is also very crucial (pure red cell aplasia).
Hepatitis E virus serology and virus PCR appear to be crucial, including virus genotype analysis if available, and considering geographical differences. Hepatitis E virus may cause more severe hepatitis-like syndrome and chronic disease if transmitted via bone marrow transplant or blood transfusion. Vidarabine-refractory cases are more common in this setting and require careful consultation with a hepatologist on how to proceed. Screening for the hepatitis E virus seems to be a more settled matter. Although vidarabine therapy is usually successful in eradicating persistent viruses, some cases may still relapse. Repeat therapy with vidarabine might be an effective solution. It is crucial to gather more information about how well vidarabine works and how frequently it can be administered to at-risk patients, especially after transplants. However, in cases of post-transplant HEV, repeated vidarabine treatment only works in about half of the patients [26,28,29].
Patients receiving bone marrow transplants are more vulnerable to infections caused by Entamoeba histolytica, Cryptosporidium, and Giardia. Reports are also emerging of an increasing number of zoonotic cases [42,43,44].

Cooled Platelet Issue

Red blood cell transfusion is essential in nearly all bone marrow transplant cases, with the well-known but not excessively high risk of pathogen transmission [45]. Platelet transfusions are administered in large quantities and frequently to bone marrow transplant patients, as platelet count recovery is slower after transplantation compared to other cell lines (50-100 Units). Platelet transfusion presents a greater risk of pathogen transmission than RBC transfusion, primarily due to the very short incubation time needed to achieve optimal platelet function.
The risk is significantly higher with platelet transfusions, which is a significant concern in oncohaematology and bone marrow transplant patient care. The estimated transmission rate of Bacterial infections occur in 1 in 2,000–5,000 units of platelet transfusions from pooled whole-blood-derived platelets and 1 in 15,000 units from single-donor apheresis preparations [44,45,46]. This notable difference mainly results from storing platelet products at room temperature (22 ± 2 °C).
Biological differences: Cooled temperature-prepared platelets are cleared from circulation much faster than standard temperature platelets. They bind to glycoprotein receptors, activating clotting on the vascular wall surface directly. Formation occurs quickly and is more effective in acute bleeding, but is less potent in maintaining platelet counts within the required range. Anyway, pathogen transmission is lower with cooled prepared platelets. Platelet thawing and in vitro culture are promising methods to reduce the risk of pathogen transmission, and efforts are ongoing to preserve their functional activity [47,48,49].

Viral Reactivations Following Bone Marrow Transplantation

Post-bone marrow transplant viral reactivations can lead to two types of serious problems. Type 1: Viral disease is active, causing illness, clinical signs, and potentially leading to critical or severe symptoms [51]. Good examples include reactivation of Cytomegalovirus, BK, RS, and EBV viruses. Type 2: Other viruses can also impair the function of the bone graft or cause graft loss, and may induce GVHD, such as adenovirus, RS virus, parvovirus B19, and cytomegalovirus. These facts underscore the importance of regular monitoring, particularly when clinical signs are present [52,53].

Conclusions

Sickle cell disease is a condition that can significantly impact various aspects of health, leading to a wide range of potentially life-threatening complications. These include vascular events, hypo-asplenia, and impaired immune system function. The disease often results in a lower quality of life and a shorter life expectancy for those affected. To manage and prevent vaso-occlusive complications, regular transfusions are essential. There is also an increased risk of:
-
multitransfusion
-
increased susceptibility to a series of infectious diseases, some of which may be bloodborne
-
unusual clinical course (e.g. parvovirus B19, hepatitis E virus)
-
The presence of blood group antibodies necessitates extra caution during serological matching procedures. Special attention is essential for bloodborne or other transmitted infections involving traditionally recognised agents, as well as for rare donorderived infection risks, based on new data concerning the presence of some blood group alloantigens.
Organ and bone marrow stem cell transplantation share transmission risks with many common pathogens, zoonoses, and other unexpected infections. The shorter period between donor death and transplantation in non-living (brain death or cadaver) organs leaves less time for various in vitro tests. Therefore, lifestyle details and geographical differences become even more critical. Hepatitis E virus poses a serious problem for all transplant patients. Cooled platelets offer an attractive method for reducing pathogen transmission through platelet transfusions, particularly in the large volumes used in bone marrow transplant settings. However, many details remain unclear and require further experience. Viral reactivation shows similarities, but also significant differences, among patient groups undergoing organ or bone marrow transplantation.

Declaration of Independence

This review did not receive any industrial support and was not modified by any other organisations.

Abbreviations

HbS mutated haemoglobin in Sickle Cell Disease
HEV, HBV, HCV hepatitis E, B, C virus
HTLV human T-lymphotropic virus (HIV)
RBC Red Blood Cell
SCD sickle cell disease

References

  1. Ogbaselase-Beck FA, Williams-Kirkwood W, Johal S et al. Medical and socioeconomic outcomes in pediatric Sickle Cell disease. 2025 Clin Pediatr 6:858-866.
  2. Gann G and Sickle Cell Disease coordinators. Global, regional and national prevalence and mortality burden of sickle cell disease 2000,-2021 Lancet Haematology 2023 10, 22-35. [CrossRef]
  3. Smith-Whitley K, Hassel KA. Clinical outcomes associated with SCD Ann Intern Med 2018 169:619-624. [CrossRef]
  4. Mekontso Dessap A, Dauger S, Khellaf M et al Guidelines for the management of emergencies and critical illness in pediatric and adult patients with sickle cell disease. Ann Intensive Care 2025 15:74-85. [CrossRef]
  5. Howard J, Thein SL. Optimal disease management and health monitoring in adults with SCD Haematology, Am Soc Hematol Educ Prog 2019 1:505-512 Suund P. [CrossRef]
  6. Ilonze C, Echefu GC, Broadnax AL et al. Cardiovascular complications of sickle cell disease: A primer for the general clinician. Natl Med Assoc 2024 116:517-525. [CrossRef]
  7. Galdwin MT, Bovelli EM. Pathophysiology of SCD. Annu Rev Pathol 2019.14:163-292.
  8. Suund P, Galdwin MT, Bovelli EM. Pathophysiology of SCD Annu. Rev Pathol 2019 14:263-292.
  9. Peretz S, Lishits L, Pretorius E et al The protective effect of the spleen in SCD, comparative study between patients with asplenia, hyposplenia and hypersplenism. Front physiol. 2007, 219:339-242.
  10. Gemmete JJ, Davagnanm I, Toma AW et al Arterial ischaemic stroke in children. Neuroimaging Clin N Am 201311:124-128.
  11. Hoz JA, Otones LL, Saenz H etal. Parvovirus B19 infection in children with SCD, watch out for splenomegaly Afr Health Sci 2022 2:598-6013.
  12. Lobo C, Silva-Pinto AC, Cançado RD et al. Optimisation of hydroxyurea in sickle cell disease in Brazil Hematol Transfus Cell Ther. 2025 Apr-Jun, e103836, electronic publication.
  13. Ball J, Bradley A, Le A, Tisdale JF. Current and future treatments for sickle cell disease: From hematopoietic stem cell transplantation to in vivo gene therapy. Mol Ther. 2025 33:2172-2191. [CrossRef]
  14. Okpala I, Nonyelu C, Muoghalu E. et al Preclinical therapeutics for sickle cell disease: modern developments and future considerations. Expert Opin Investig Drugs. 2025 34:301-315. [CrossRef]
  15. Blatyta PF, Kelly S, Sabino E et al. Prevalence of serologic markers of transfusion and sexually transmitted infections and their correlation with clinical features in a large cohort of Brazilian patients with sickle cell disease.Epidemiology and Donor Evaluation Study II, Brazil. Transfusion. 2020 60:343-350. [CrossRef]
  16. Ochocinski D, Dalal M, Black LV et al. Life-Threatening Infectious Complications in Sickle Cell Disease: A Concise Narrative Review..Front Pediatr. 2020 Feb 20:38:e42 electronic publication. [CrossRef]
  17. Hoz JA, Otones LL, Saenz H. et al. Parvovirus B19 in children with with SCD, watch out for splenomegaly. Afr Heath Sci 2022 2:598-601. [CrossRef]
  18. Riviere S: British Society for Haematology guidelines to improve care of asplenic patients, Much to be done. J Haematol 2024 204:1573. [CrossRef]
  19. Deeb M, Leung KK, Ward R, et al Hepatobiliary complications in patients with sickle cell disease: A 30-year review of 1009 patients.Hepatol Commun. 2025 in press, electronic. [CrossRef]
  20. Yang J, Qi JL, Wang XX, Li XH, Jin R, Liu BY, Liu HX, Rao HY. The burden of hepatitis C virus in the world, China, India, and the United States from 1990 to 2019. Front Public Health. 2023 Mar 2;11:1041201. [CrossRef] [PubMed] [PubMed Central]
  21. Rzymski P, Jibril AT, Rahmah L, Abarikwu SO, Hashem F, Lawati AA, Morrison FMM, Marquez LP, Mohamed K, Khan A, Mushtaq S, Minakova K, Poniedziałek B, Zarębska-Michaluk D, Flisiak R. Is there still hope for the prophylactic hepatitis C vaccine? A review of different approaches. J Med Virol. 2024 Sep;96(9):e29900. [CrossRef] [PubMed]
  22. (Arend P. (2021). Why blood group A individuals are at risk. In contrast, blood group O individuals are protected from SARS-CoV-2 (COVID-19) infection: A hypothesis regarding how the virus invades the human body via ABO(H) blood group-determining carbohydrates. Immunobiology, 226(3), 152027. [CrossRef]
  23. Vichinsky E. P. (2001). Current issues with blood transfusions in sickle cell disease. Seminars in hematology, 38(1 Suppl 1), 14–22. [CrossRef]
  24. Daniels G. (1997). Blood group polymorphisms: molecular approach and biological significance. Transfusion clinique et biologique : journal de la Societe francaise de transfusion sanguine, 4(4), 383–390. [CrossRef]
  25. Fasano, R. M., Meyer, E. K., Branscomb, J., White, M. S., Gibson, R. W., & Eckman, J. R. (2019). Impact of Red Blood Cell Antigen Matching on Alloimmunization and Transfusion Complications in Patients with Sickle Cell Disease: A Systematic Review. Transfusion medicine reviews, 33(1), 12–23. [CrossRef]
  26. Wising MH, Meirter TL, Nocke k et al Genetic determinants of host-virus derived insertions for hepatitis E replication Nat Commun 2024 15 4855-4863. [CrossRef]
  27. Melchert J, Radbruch H Haits LG et al. Whole genome sequencing reveals insights into HEV genome diversity and virus compartmentalisation in chronic hepatitis E. J Clin Virol 2023 168. 883-899. [CrossRef]
  28. Kogias D. Gravilidis E Antonideau C.Hepatitis E infection in immunocompromised patients previously treated with rituximab J Viral hepat 2025 Mar e7705 electronic publication.
  29. Nanmoku K, Owada Y Oshiro et al. Prevalence and characteristics of HEV in kidney transplant patients, single-centre evidence in Japan. Transpl Infect Dis. 2019, April 21:e13033, electronic publication. [CrossRef]
  30. Dutch M, Patrick CJ, Boan PA, et al. Prevalence of Blood-borne Viruses and Predictors of Risk in Potential Organ Donors in Australia. Transpl. int. 2022. 35:10395-10399. [CrossRef]
  31. Kirchner VA, Pruett TL: Receiving an unwanted gift, infection through organ transplantation. Surg Infect 2016 17:218-322. [CrossRef]
  32. Singhe R, Habachou LI, Craig JC et al. Unexpected donor-derived transmissions by kidney transplantation: a systematic review. Transplant Cell Ther.v2022,e28408, electronic publication. [CrossRef]
  33. Lau KCK, Oslowy C Giles E et al. Deep sequencing shows low-level oncogenic hepatitis B virus variants persist post-liver transplant despite potent anti-HBV prophylaxis. J Viral Hepat 2018 25:724-732. [CrossRef]
  34. Rosen A. Ison MG. Screening of living donors for endemic infections, understanding the challenges and benefits of enhanced screening. Transpl Infect Dis 2017 Feb 19: e12633, electronic publication.
  35. Saha A, Browning SA, Dandfamudi R. Donor-derived Ehrlichiosis 2 clusters following solid organ transplantation. Clin Infect Dis 2022 74:9018-923. [CrossRef]
  36. Wojcziech W, Sulima M, Benke M: Parasitic infections associated with unfavourable outcomes in transplant recipients. Medicina (Kaunas) 2018 54:27-32. [CrossRef]
  37. Hague E, Muhsen IN Rasheed W.Parasitic infections in haemopoetic stem cell transplant recipients. Transp Infect Dis. 2023 Nov Suppl 1e1460, electronic publication.
  38. Yamauchi J, Raghavan D, Imlay . Decreased organ Donor HTLV Screening Practices post-elimination of universal screening in the US. Transplant Direct 2024 1010:e1707electronic publication.
  39. Zhang J, Lin J, Tian Y. Transmission of rabies through solid organ transplantation, a notable problem in China. BMC Infect Dis 2018 18:273-278. [CrossRef]
  40. Tutschka PJ. Infections and immunodeficiency in bone marrow transplantation Pediatr Infect Dis 1988 May supplement 5: S22-S29.
  41. MrzliakA, Novak R, Pandak N. Emerging and neglected zoonoses in transplant population. World J Transplant 2020 10:47-63. [CrossRef]
  42. Galli M, Masina L, Magliano G. Neurotoxoplasmosis in haploidentical haematopoietic stem cell transplantation. Ann Hematol. 2025, 104:2527-2528. [CrossRef]
  43. Gatault P, Aé-Haji S, Noble J. CMV-infected kidney grafts drive the expansion of blood-borne CMV-specific T cells restricted by shed class I molecules via presentation on donor cells. MJ Transplant (:1904-19132018. [CrossRef]
  44. Udvardy M. Illes A, Gergely L. Transfusion transmitted disorders 2023 with special attention to Bone Marrow Transplant Patients. Pathogens 202312:901-909. [CrossRef]
  45. (Sanz, C., Pereira, A., Vila, J., Faundez, A. I., Gomez, J., & Ordinas, A. (1997). Growth of bacteria in platelet concentrates obtained from whole blood stored for 16 hours at 22°C before component preparation. Transfusion, 37(3), 251–254. [CrossRef]
  46. (Levy JH, Neal MD, Herman JH. Bacterial contamination of platelets for transfusion: strategies for prevention. Crit Care. 2018 Oct 27;22(1):271. [CrossRef] [PubMed] [PubMed Central]
  47. (Rumjantseva V, Hoffmeister KM. Novel and unexpected clearance mechanisms for cold platelets. Transfus Apher Sci. 2010 Feb;42(1):63-70. Epub 2009 Nov 20. [CrossRef] [PubMed] [PubMed Central]
  48. (Rothwell, S. W., Maglasang, P., Reid, T. J., Gorogias, M., & Krishnamurti, C. (2000). Correlation of in vivo and in vitro functions of fresh and stored human platelets. Transfusion, 40(8), 988–993. [CrossRef]
  49. Martínez-Botía, P., Acebes-Huerta, A., Seghatchian, J., & Gutiérrez, L. (2020). In vitro platelet production for transfusion purposes: Where are we now?. Transfusion and apheresis science : official journal of the World Apheresis Association : official journal of the European Society for Haemapheresis, 59(4), 102864. [CrossRef]
  50. Düver F, Weißbrich B, Eyrich M, Wölfl M, Schlegel PG, Wiegering V. Viral reactivations following hematopoietic stem cell transplantation in pediatric patients - A single center 11-year analysis. PLoS One. 2020 Feb 4;15(2):e0228451. [CrossRef] [PubMed] [PubMed Central]
  51. Important CMV, EBV, Adeno, RS viralreactivation, maybe lifer threatening, and damages bone marrow, may provoke rejection and influence GVHD.
  52. BK virus reactivation is quite common (also in kidney transplanted patients), standard diagnosis and therapy is much.
  53. Wang Z, Vathsala A, Tiong HY. Haematuria in postrenal transplant patients. Biomed Res Int. 2015;2015:292034. Epub 2015 Mar 30. [CrossRef] [PubMed] [PubMed Central]
Disclaimer/Publisher’s Note: The statements, opinions and data contained in all publications are solely those of the individual author(s) and contributor(s) and not of MDPI and/or the editor(s). MDPI and/or the editor(s) disclaim responsibility for any injury to people or property resulting from any ideas, methods, instructions or products referred to in the content.
Copyright: This open access article is published under a Creative Commons CC BY 4.0 license, which permit the free download, distribution, and reuse, provided that the author and preprint are cited in any reuse.
Prerpints.org logo

Preprints.org is a free preprint server supported by MDPI in Basel, Switzerland.

Subscribe

Disclaimer

Terms of Use

Privacy Policy

Privacy Settings

© 2025 MDPI (Basel, Switzerland) unless otherwise stated