Francis Cedrick J.

Victorino
423
MD 4Y2 1
2016

CPAP
February

26,

EPSTAIN-BARR VIRUS IN SYSTEMIC AUTOIMMUNE DISEASE (Draborg et. al,

2013)
Systemic autoimmune diseases (SADs) include several autoimmune-related
disorders characterized by overlapping clinical symptoms and characteristic
antibodies caused by multifactorial factors (both genetic and environmental).
Incidence of genetic SADs are observed on monozygotic twins and those related to
genes of major histocompatibility complex (MHC). SADs caused by environmental
factors are commonly observed in infection, including Epstain-Barr virus (EBV) which
is the focus of this study. This journal links Epstain-barr virus infection in most
extensively studied SADs, Systemic lupus erythematosus (SLE), rheumatoid arthritis
(RA) and Sjgrens syndrome (SS). Epstain-barr virus is an infectious DNA virus of
the herpes family comprising of a linear dsDNA genome enclosed with icosahedral
capsid surrounded by host cell membrane-derived envelope implanted with
glycoproteins. EBV infection is transmitted in saliva primarily infecting the epithelial
cells of the orophanynx and nasopharynx. Consequently, enters the underlying
tissues and infecting B-cells.
Several studies linked EBV to the development of SLE. 42% of SLE patient
were found to have elevated level of EBV DNA antigens in their serum, this findings
on increased EBV load are suggestive of active lytic replication in SLE patient. This
suggests that re-infection with EBV is related with SLE development. The journal
suggests that an SLE patient have an elevated viral load, increased EBV mRNA
expression, increased EBV antibodies, and depressed immunity with EBV compared
to healthy control.
EBV in RA has long been assumed to have a role in RA pathogenesis. EBV
DNA/RNA antigens are present on some but relative cells/fluids of RA patient
demonstrated by the use of in-situ hybridization and PCR. Moreover, 10-fold higher
degrees of EBV-infected B cells are observed in RA patient compared to healthy
controls. Also, EBV-DNA antigens are present in synovial tissue plasma cell
producing CCP (cyclic citrulinated peptide) antibodies of RA patients implying EBVinfected cells has a role in synovial inflammation of RA patient.
Increased EBV viral load (in saliva and lacrimal glands of SS patient) and EBV
antibodies are also associated with Sjogrens syndrome (SS) thus suggesting a
connection with EBV infection. Additionally, SS patient are known to have increased

risk of developing EBV-associated lymphomas. One study has shown that saliva of
SS patient can activate EBV.
The study concluded that EBV is demonstrated to have a role as an
environmental factor that triggers development of SADs, most commonly SLE, RA
and SS.

HYPERSENSITIVITY
PNEUMONITIS:
PATHOBIOLOGY (Selman et. al, 2013)

INSIGHTS

IN

DIAGNOSIS

AND

Hypersensitivity pneumonitis (HP) is a syndrome caused by relatively small

particle enough to reach the alveoli, these particles may be fungal, bacterial, animal
and insect proteins; and low molecular weight chemical compounds. Susceptible
individuals demonstrate an exaggerated immune response following antigen
exposure. Though there is a wide range of offending antigens that can stimulate
hypersensitivity pneumonitis, only few individuals develop the disease. In lieu of
this, a two-hit hypothesis is suggested which states that preexisting susceptibility or
environmental factors increases the risk for the development of HP after contact
with antigen which regards antigens as the inducing factor and the genetic or
environmental factors act as promoting risk factor. HP antigens are universal and
widely distributed, the most commonly implicated antigens are themophilic
antinomycetes,
fungi
and
bird
proteins.
Thermophilic
actinomycetes
(Saccharopolyspora rectivirgula) and number of fungi (Aspergillus and Penicillium
species) are usually caught up in farming industries and also home environments.
High and low molecular weight proteins from avians demonstrates the bird
fanciers lung also called pigeon-breeders lung. Mycobacterium avium complex
colonization in heated water usually shows high incidence thus causing HP.
Several factors are known to promote the development of the disease, like
genetic susceptibility and environmental factors as stated above and some factors
are known to protect the host from developing the infection. Genetic susceptibility,
given its role in regulating immune response, a focus has been placed on the major
histocompatibility complex (MHC). High level of MHC polymorphism and
heterozygosity offer the immune system with a selective advantage against
pathogen diversity but it adds risks of generating diverse immunopathological
disorders. Likewise, an environmental promoting factor like respiratory viral
infection and high pesticide exposure were strongly associated with a diagnosis of
HP. Cigarette smoking demonstrates an inconsistent role in HP development. It is
said that HP is less frequent in smokers than in nonsmokers under the same risk of
exposure, the mechanism by which cigarette smoke protects from HP are unclear,
but several experimental studies shows that this paradoxical effect is caused by
nicotine. Immune tolerance also act as a protective factors, it is shown that many

exposed individuals develop a mild lymphocytic alveolitis but remain asymptomatic,

suggesting the development of tolerant response to HP antigens.