Cytomegalovirus Structure and Characteristics

Cytomegalovirus

• Cytomegalovirus belongs to the herpes virus family, beta subfamily, and has a worldwide occurrence with latency as a hallmark.
• The structure of CMV consists of a spherical shape with icosahedral symmetry, an electron-dense core, and a double-stranded DNA genome.
• The envelope is lipoprotein, trilaminar, and has viral glycoproteins spikes that bind to specific host receptors, mediating virus entry.
• The tegument is an outer proteinaceous layer that redirects host cellular proteins and enzymes to involve in viral nucleic acid replication.
• The life cycle of CMV involves assembly in nuclear viral factories, budding into intracellular vesicles, and release through exocytosis at the plasma membrane.

Pathogenesis of Human Cytomegalovirus

• The primary site of multiplication is epithelial cells of gland and mucosal tissue, smooth muscle cells, fibroblasts, macrophages, dendritic cells, hepatocytes, and vascular endothelial cells.
• The virus has a broad tropism for cells, facilitating systemic and inter-host spread.
• Primary replication occurs in mucosal epithelium, followed by prolonged secretion of virus in saliva for months, and dissemination via leukocyte leading to viremia and systemic spread.
• Latency is established in myeloid cells of the bone marrow, resulting in life-long infection with sporadic reactivation.

Pathophysiology of Latency

• The host immune response following primary HCMV infection is effective at stopping virus replication and dissemination, but the virus is never cleared by the host.
• Persistence is due to the ability of HCMV to establish latency in myeloid cells and circulating monocytes.
• Reactivation leads to infection of myeloid progenitors, resulting in latent infection in e.g., CD34+ bone marrow progenitor cells.

Clinical Manifestations

• In immunocompetent adults, CMV infection is often asymptomatic or mild and self-limiting, but can cause an acute CMV infection or "CMV mononucleosis" with fever, malaise, and enlarged lymph nodes.
• In immunosuppressed individuals, CMV infection can cause life-threatening diseases such as CMV retinitis, pneumonia, esophagitis, colitis, hepatitis, and encephalitis.
• Congenital CMV infection can cause CNS abnormalities, choroidoretinitis, sensorineural deafness, hepatosplenomegaly, pneumonitis, and other symptoms.

Treatment and Prevention

• Ganciclovir and foscarnet are used to treat life-threatening CMV infection in immunocompromised patients.
• Acyclovir and valacyclovir are used to treat bone marrow and renal transplant patients.
• Isolation of newborns with generalized cytomegalic inclusion disease, screening of transplant donors and recipients for CMV antibody, and human IgG prophylaxis in transplant recipients are measures to prevent and control CMV infection.

Mumps Virus

• Mumps virus is a pleomorphic, spherical virus with a ribonucleoprotein complex, negative-sense, unsegmented, single-stranded RNA genome.
• The virus has a nucleocapsid, envelope, and associated proteins such as large (L) protein, polymerase phosphoprotein (P) protein, nucleoprotein (NP) protein, and matrix (M) protein.
• The envelope contains two glycoproteins: hemagglutinin-neuraminidase (HN) protein and fusion (F) protein.
• Mumps virus is endemic worldwide, with the highest incidence in children aged 5-9 years, and is a vaccine-preventable disease with a live virus vaccine.