Gestational hypertension or pregnancy-induced hypertension (PIH) is the development of new hypertension in a pregnant woman after 20 weeks gestation without the presence of protein in the urine or other signs of pre-eclampsia. Gestational hypertension is defined as having a blood pressure 
greater than 140/90 on two occasions at least 6 hours apart. Signs and symptoms
No single diagnostic test currently exists to predict the likelihood of developing gestational hypertension. High blood pressure is the major sign in diagnosing gestational hypertension. Some women with gestational hypertension may present asymptomatic, but a number of symptoms are associated with the condition. [1]
Symptoms

Edema
Sudden weight gain
Blurred vision or sensitivity to light
Nausea and vomiting
Persistent headaches
Increased blood pressure

Risk factors
Maternal causes

Obesity
Mothers under 20 or over 40 years old
Past history of diabetes mellitus, hypertension (particularly gestational hypertension) and renal disease
Pre-existing hypertension
Thrombophilias (anti-phospholipid syndrome, protein C/S deficiency, factor V Leiden)
Having donated a kidneyPregnancy

Multiple gestation (twins or triplets, etc.) Placental abnormalities:
Hyperplacentosis: Excessive exposure to chorionic villi
Placental ischemiaFamily history

Family history of pre-eclampsia

Diagnosis
Conditions
There exist several hypertensive states of pregnancy:

Gestational hypertension
Gestational hypertension is usually defined as having a blood pressure higher than 140/90 measured on two separate occasions, more than 6 hours apart, without the presence of protein in the urine and diagnosed after 20 weeks of gestation. Pre-eclampsia
Pre-eclampsia is gestational hypertension plus proteinuria (>300 mg of protein in a 24-hour urine sample). Severe pre-eclampsia involves a blood pressure greater than 160/110, with additional medical signs and symptoms. HELLP syndrome is a type of pre-eclampsia.
Both sets of repeats share a region of a few hundred bps, the so-called "a sequence"; the other regions of the repeats are sometimes referred to as "b sequence" and "c sequence". Life cycle
Viral replication is nuclear and lysogenic. Entry into the host cell is achieved by attachment of the viral glycoproteins to host receptors, which mediates endocytosis. Replication follows the dsDNA bidirectional replication model. DNA templated transcription, with some alternative splicing mechanism is the method of transcription. Translation takes place by leaky scanning. The virus exits the host cell by nuclear egress, and budding. Humans and monkeys serve as the natural hosts. Transmission routes are dependent on coming into contact with bodily fluids (such as saliva, urine, and genital secretions) from an infected individual. All herpesviruses share a characteristic ability to remain latent within the body over long periods. Although they may be found throughout the body, CMV infections are frequently associated with the salivary glands in humans and other mammals. Genetic engineering
The CMV promoter is commonly included in vectors used in genetic engineering work conducted in mammalian cells, as it is a strong promoter and drives constitutive expression of genes under its control. History
Cytomegalovirus was first observed by German pathologist Hugo Ribbert in 1881 when he noticed enlarged cells with enlarged nuclei present in the cells of an infant. Years later, between 1956 and 1957, Thomas Huckle Weller together with Smith and Rowe independently isolated the virus, known thereafter as "cytomegalovirus".