Cytomegalovirus infection after transplant (NORD)

Last updated: December 18, 2025

Cytomegalovirus infection after transplant (NORD)

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Thymus histology
Spleen histology
Lymph node histology
Introduction to the immune system
Cytokines
Innate immune system
Complement system
T-cell development
B-cell development
MHC class I and MHC class II molecules
T-cell activation
B-cell activation, differentiation, and contraction
Cell-mediated immunity of CD4 cells
Cell-mediated immunity of natural killer and CD8 cells
Antibody classes
Somatic hypermutation and affinity maturation
VDJ rearrangement
Contracting the immune response and peripheral tolerance
B- and T-cell memory
Anergy, exhaustion, and clonal deletion
Vaccinations
Type I hypersensitivity
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Type III hypersensitivity
Type IV hypersensitivity
Sepsis
Neonatal sepsis
Abscesses
Food allergy
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Asthma
Immune thrombocytopenia
Autoimmune hemolytic anemia
Hemolytic disease of the newborn
Rheumatic heart disease
Myasthenia gravis
Graves disease
Pemphigus vulgaris
Serum sickness
Systemic lupus erythematosus
Poststreptococcal glomerulonephritis
Graft-versus-host disease
Contact dermatitis
Transplant rejection
Cytomegalovirus infection after transplant (NORD)
Post-transplant lymphoproliferative disorders (NORD)
X-linked agammaglobulinemia
Selective immunoglobulin A deficiency
Common variable immunodeficiency
IgG subclass deficiency
Hyperimmunoglobulin E syndrome
Isolated primary immunoglobulin M deficiency
Thymic aplasia
DiGeorge syndrome
Severe combined immunodeficiency
Adenosine deaminase deficiency
Ataxia-telangiectasia
Hyper IgM syndrome
Wiskott-Aldrich syndrome
Leukocyte adhesion deficiency
Chediak-Higashi syndrome
Chronic granulomatous disease
Complement deficiency
Hereditary angioedema
Asplenia
Thymoma
Ruptured spleen
Immunodeficiencies: T-cell and B-cell disorders: Pathology review
Immunodeficiencies: Combined T-cell and B-cell disorders: Pathology review
Immunodeficiencies: Phagocyte and complement dysfunction: Pathology review
Glucocorticoids

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Cytomegalovirus, or CMV, is an enveloped double-stranded DNA virus that belongs to the herpesviridae family. It's one of the most common viruses to cause severe infection in individuals undergoing transplantation of bone marrow or solid organs like the liver or kidney. It can affect almost every organ in the body resulting in encephalitis, retinitis, pneumonia, hepatitis, gastroenteritis, and of course, transplant rejection.

In the post-transplantation period, the recipient is usually given immunosuppressive medication in order to prevent their immune system from recognizing the transplanted tissue as foreign and causing rejection. However, one major disadvantage of this approach is that the weakened immune system is unable to protect the body against pathogens like CMV.

CMV can be transmitted through blood and other body fluids like saliva, genital secretions, and urine of an infected person; or from the transplanted organ itself!

During the primary infection, the virus usually invades the epithelial cells, like those that make up the oral, GI, or urinary mucosa; and starts to multiply. CMV damages the infected cells by breaking down the cytoskeletons which maintain the cell structure. That results in enlarged cells with intranuclear viral inclusion bodies, giving it the typical owl's eye appearance.

CMV also infects monocytes in the blood and sets up a latent infection, which means that the virus remains dormant for long periods of time. The dormant virus can reactivate at times when the immune system weakens, causing disease.

Most of the time primary infection occurs years before the transplant with resultant  reactivation of the virus during immunosuppressive therapy. In about 25% of transplants primary infection occurs which is usually much more severe compared to reactivation.