Cause
Common causes of viral pneumonia are:

Influenza virus A and B
Respiratory syncytial virus (RSV)
Human parainfluenza viruses (in children)
Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2)Rarer viruses that commonly result in pneumonia include:

Adenoviruses (in military recruits)
Metapneumovirus
Severe acute respiratory syndrome coronavirus (SARS-CoV)
Middle East respiratory syndrome virus (MERS-CoV)
HantavirusesViruses that primarily cause other diseases, but sometimes cause pneumonia include:

Herpes simplex virus (HSV), mainly in newborns or young children
Varicella-zoster virus (VZV)
Measles virus
Rubella virus
Cytomegalovirus (CMV), mainly in people with immune system problems
Smallpox virus
Dengue virusThe most commonly identified agents in children are respiratory syncytial virus, rhinovirus, human metapneumovirus, human bocavirus, and parainfluenza viruses. History
In the pre-antibiotic age, pneumonias had been treated with specific anti-serums of highly variable therapeutic effect and undesirable side-effects (a practice eliminated by the advent of sulfamides in 1936 and the beginning availability of penicillin in the 1940s). Viral pneumonia was first described by Hobart Reimann in 1938, in an article published by JAMA, An Acute Infection of the Respiratory Tract with Atypical Pneumonia: a disease entity probably caused by a filtrable virus. Reimann, Chairman of the Department of Medicine at Jefferson Medical College, had established the practice of routinely typing the pneumococcal organism in cases where pneumonia presented. Out of this work, the distinction between viral and bacterial strains was noticed. Pathophysiology
Viruses must invade cells in order to reproduce. Typically, a virus will reach the lungs by traveling in droplets through the mouth and nose with inhalation. There, the virus invades the cells lining the airways and the alveoli.
Waldenström macroglobulinemia cells show only minimal changes in cytogenetic and gene expression studies. Their miRNA signature however differs from their normal counterpart. It is therefore believed that epigenetic modifications play a crucial role in the disease.Comparative genomic hybridization identified the following chromosomal abnormalities: deletions of 6q23 and 13q14, and gains of 3q13-q28, 6p and 18q. FGFR3 is overexpressed. The following signalling pathways have been implicated:

CD154/CD40
Akt
ubiquitination, p53 activation, cytochrome c release
NF-κB
WNT/beta-catenin
mTOR
ERK
MAPK
Bcl-2The protein Src tyrosine kinase is overexpressed in Waldenström macroglobulinemia cells compared with control B cells. Inhibition of Src arrests the cell cycle at phase G1 and has little effect on the survival of Waldenström macroglobulinemia or normal cells. MicroRNAs involved in Waldenström:
increased expression of miRNAs-363*, -206, -494, -155, -184, -542–3p. decreased expression of miRNA-9*.MicroRNA-155 regulates the proliferation and growth of Waldenström macroglobulinemia cells in vitro and in vivo, by inhibiting MAPK/ERK, PI3/AKT, and NF-κB pathways.In Waldenström macroglobulinemia cells, histone deacetylases and histone-modifying genes are de-regulated. Bone marrow tumour cells express the following antigen targets CD20 (98.3%), CD22 (88.3%), CD40 (83.3%), CD52 (77.4%), IgM (83.3%), MUC1 core protein (57.8%), and 1D10 (50%). Pathophysiology
Symptoms including blurring or loss of vision, headache, and (rarely) stroke or coma are due to the effects of the IgM paraprotein, which may cause autoimmune phenomenon or cryoglobulinemia. Other symptoms of Waldenström macroglobulinemia are due to hyperviscosity syndrome, which is present in 6–20% of patients.