Viral pneumonia is a subset of the pneumonitides, which were at one time called atypical pneumonias.

In the
past, all pneumonias were labeled atypical if a bacterial pathogen could not be identified with Gram staining
and if the pneumonia did not respond to antibiotics.

Viral pneumonia is defined as a disease in which there are gas exchange

abnormalities at the alveolar level accompanied by inflammation of the lung
parenchyma.
Currently, 1,200 viruses that infect the respiratory tract are known to exist,
although many of them are not likely to cause disease.(1)
In recent years, severe acute respiratory syndrome (SARS) coronaviruses, avian
H5N1 influenza A viruses and North American hantaviruses have gained prominence
as causative agents of severe pneumonia
viruses impair the local respiratory tract defense mechanisms by damaging the
respiratory tract mucosa, thereby favoring the onset of secondary bacterial
pneumonia. In addition, some chronic diseases, such as COPD and heart failure, and
even pregnancy have been described as being associated with a greater risk of viral
pneumonia.(3)
Influenza A and B, RSV, parainfluenza, metapneumovirus, coronavirus, rhinovirus,
hantavirus and adenovirus are among the viruses that cause community-acquired
pneumonia.
(Viral pneumonia: epidemiological, clinical, pathophysiological and therapeutic
aspects* Pneumonias virais: aspectos epidemiolgicos, clnicos, fisiopatolgicos e
tratamento Luiz Tadeu Moraes Figueiredo, J Bras Pneumol. 2009;35(9):899-906)
There are four types of influenza viruses that cause seasonal flu in humans: two influenza A
viruses (H3N2 and H1N1) and two influenza B viruses (Yamagata and Victoria). While H3N2
viruses are the most common of the seasonal influenza viruses, H1N1 and B viruses also cause
epidemics worldwide each year. The WHO selects representative strains of all four A and B
viruses for inclusion in the seasonal influenza vaccine each year.
Senior author Dr Colin Russell, from the Department of Veterinary Medicine at the University of
Cambridge, UK, said: While H3N2 viruses die out between epidemics and new viruses emerge
from east and southeast Asia every year, H1N1 and B viruses frequently circulate continuously
between epidemics worldwide. This continuous circulation gives rise to a huge diversity in H1N1
and B viruses circulating globally.( Nature 523,217220 (09 July 2015))

Pneumonia etiology studies that incorporate viral studies show that respiratory syncytial virus is the
leading viral cause, being identified in 1540% of pneumonia or bronchiolitis cases admitted to hospital in
children in developing countries, followed by influenza A and B, parainfluenza, human metapneumovirus
and adenovirus.38,61,62 (http://www.who.int/bulletin/volumes/86/5/07-048769/en/)

Epidemiology
Various studies have reported differing frequencies of the other viruses causing community-acquired
pneumonias, with RSV ranging from 1-4%, adenovirus 1-4%, PIV 2-3 %, hMPV 0-4%, and coronavirus 1-14%
of pathogen-diagnosed pneumonia cases

T]he most common CT finding in hospitalized patients with MERS-CoV infection is that of bilateral
predominantly subpleural and basilar airspace, with more extensive ground-glass opacities than
consolidation," the authors conclude. "The predilection of the abnormalities to the subpleural and
peribronchovascular regions is suggestive of an organizing pneumonia pattern. Recognizing this pattern
in acutely ill patients living in or traveling from endemic areas may help in the early diagnosis of MERSCoV infection(American Journal of Roentgenology. 2014;203: 782-787)
http://america.aljazeera.com/articles/2014/5/27/mers-spreads-iran.html

Schematic representation of influenza virus replication cycle

and sites of action of antiviral agents. Note.Influenza A virus
contains eight RNA segments of negative polarity coding for at
least 11 viral proteins. The surface proteins of influenza A
virus consist of two glycoproteins, hemagglutinin (HA) and
neuraminidase (NA), and the M2 protein. The HA protein
attaches the virus to sialic acidcontaining receptors on the
cell surface and initiates infection. A fusion protein inhibitor
(DAS-181) targets the influenza virus receptor in the host
respiratory tract and inhibits virus attachment. Cyanovirin-N
(CVN) binds to high-mannose oligosaccharides on HA and
inhibits the entry of virus into cells. For most influenza A
viruses, the M2 ion channel blockers (amantadine and
rimantadine) impede viral replication at an early stage of
infection after penetration of the cell but prior to uncoating.
M2 blockers inhibit the decrease in pH within the virion and
thus block the release of viral RNA into the cytoplasm and
prevent transportation of the viral genome to the nucleus.
Inhibition of the viral polymerase, an essential component of
viral RNA replication in the nucleus, can be blocked by the
polymerase inhibitors ribavirin and T-705. Small interfering
RNAs (siRNAs) that target different viral genes can inhibit viral
replication. Several mechanisms of action have been proposed
for the anti-influenza virus activity of ribavirin. One is the
inhibition of the cellular enzyme inosine monophosphate
dehydrogenase, resulting in a decrease in the intracellular
guanosine 5-triphosphate (GTP) that is required for nucleic

acid synthesis. Ribavirin triphosphate also inhibits the function

of virus-coded RNA polymerases which are necessary to
initiate and elongate viral mRNAs. Late in infection, NA
cleaves sialic acidcontaining receptors and facilitates the
release of budding virions. NA inhibitors (zanamivir,
oseltamivir, peramivir, and LANI) block NA activity, preventing
the release of virions from the cell.

Several years ago, the National Institute of Allergy and

Infectious Diseases (NIAID) Antiviral Study Group compared
outcomes among hospitalized adults with influenza who
received either nebulized zanamivir plus oral rimantadine or
nebulized saline placebo plus oral rimantadine [51] The
pharmacokinetics of amantadine was not affected by
coadministration of oseltamivir. Similarly, amantadine did not
affect the pharmacokinetics of oseltamivir or its metabolite,
oseltamivir carboxylate. There was no evidence of an increase
in the frequency or severity of adverse events when
amantadine and oseltamivir were used in combination [52].
T-705 (favipiravir, 6-fluoro-3-hydroxy-2-pyrazinecarboxamide).
The mode of action of ribosylated, triphosphorylated T-705 (T705 RTP) is similar to that of ribavirin triphosphate: inhibition
of influenza virus RNA polymerase [57,58]. Unlike ribavirin 5
monophosphate, T-705 RMP only weakly inhibits cellular
inosine monophosphate dehydrogenase [58,59] and thus is
less cytotoxic.
Many studies have shown that oxidative stress is important in
the pathogenesis of pulmonary damage during influenza virus
infections. Antioxidant molecules are therefore potentially
useful against viral infection. It was shown that antioxidant
molecule N-acetylcysteine (NAC) in combination with ribavirin
enhanced survival of mice against a lethal influenza virus
infection [64]. Further studies have demonstrated that

treatment of mice with NAC combined with oseltamivir

resulted in 100% survival
Long-acting inhaled NA inhibitor (LANI) is a multimeric
zanamivir compound (CS-8958) that persists longer in the lung
and can be administered once weekly. Moreover, phase II
clinical studies in Japan showed that a single inhaled dose of
LANI was as effective as a standard five-day course of
oseltamivir [71], and a double-blind, randomized, controlled
trial showed that the LANI laninamivir octanoate was effective
and well-tolerated in children with oseltamivir-resistant
influenza A (H1N1) virus infection
he influenza virus receptor inactivator DAS181 (Fludase), a sialidase fusion
protein, has shown inhibitory activity against a large number of seasonal
influenza strains and a highly pathogenic avian influenza H5N1 strain [ 73,74].
Thus far, DAS181 has been well tolerated with no serious adverse events in
phase I trials, and phase II trials have begun [75].
Other potential anti-influenza agents include Cyanovirin-N (CVN), a
carbohydrate-binding protein that inhibits viral entry into cells by specifically
binding to high-mannose oligosaccharides on the surface glycoproteins of
enveloped
viruses
[76];
small
interfering
RNAs
(siRNAs);
immunomodulators; and immunotherapy with convalescent plasma and
neutralizing antibodies.
DAS181 (Fludas) is a sialidase catalytic domain/amphiregulin glycosaminoglycan
binding sequence fusion protein that cleaves both the Neu5Ac (2,3)- and Neu5Ac
(2,6)-Gal linkages of sialic acid on host cells. DAS181 is administered as an
inhalable dry powder to deliver sialidase to the pulmonary epithelium for cleavage
of sialic acids, which renders the cells inaccessible to infection by virus [

Administration of inactivated influenza vaccine to persons receiving influenza antiviral drugs

for treatment or chemoprophylaxis is acceptable.

Live-attenuated influenza vaccine should not be administered until 48 hours after cessation
of influenza antiviral therapy.

If influenza antiviral medications are administered within 2 weeks after receipt of liveattenuated influenza vaccine, the vaccine dose should be repeated 48 or more hours after the
last dose of antiviral medication.

. For example people younger than 65 years of age should not get the high-dose flu shot and
people who are younger than 18 years old or older than 64 years old should not get the
intradermal flu shot.